5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

•Pneumonia

•Pleural effusion

•Pneumothorax

•Pulmonary infarction

•Lung cancer

•Pneumoconiosis

•Fungal diseases

•Tuberculosis

Nonpleuritic Chest Pain

Nonpleuritic chest pain is described as a constant pain that is usually located centrally. It is not generally worsened by deep inspiration. The pain also may radiate. Nonpleuritic chest pain is associated with the following disorders:

•Myocardial ischemia

•Pericardial inflammation

•Pulmonary hypertension

•Esophagitis

•Local trauma or inflammation of the chest cage, muscles, bones, or cartilage

Abnormal Chest Shape and Configuration

During inspection, the respiratory care practitioner systematically observes the patient's chest for both normal and abnormal findings. Is the spine straight? Are any lesions or surgical scars evident? Are the scapulae symmetric? Is there a barrel chest deformity? Common chest deformities are listed in Table 3.3 and illustrated in Fig. 3.21.

TABLE 3.3

Common Abnormal Chest Shapes and Configurations

Condition	Description
Kyphosis	A “hunchbacked” appearance caused by posterior curvature of the spine
Scoliosis	A lateral curvature of the spine that results in the chest protruding posteriorly and the anterior ribs
	flattening out

Kyphoscoliosis The combination of kyphosis and scoliosis (see Fig. 25.1)

Pectus	The forward projection of the xiphoid process and lower sternum (also known as “pigeon breast”
carinatum	deformity)
Pectus	A funnel-shaped depression over the lower sternum (also called “funnel chest”)
excavatum
Barrel chest	In the normal adult, the anteroposterior diameter of the chest is about half its lateral diameter, or 1 : 2.
	When the patient has a barrel chest, the ratio is nearer to 1 : 1 (see Fig. 3.21)

FIGURE 3.21 (A), Normally, the anteroposterior diameter is about half the lateral diameter (a ratio of 1 : 2). Because of the air trapping and lung hyperinflation in obstructive pulmonary diseases, the natural tendency of the lungs to recoil is decreased and the normal tendency of the chest to move outward prevails. This condition results in an increased anteroposterior diameter and is referred to as the barrel chest deformity. The ratio is nearer to 1 : 1. (B) The anteroposterior diameter commonly increases with aging. Therefore older individuals may have a slight barrel chest appearance in the absence of any pulmonary disease. Normal infants also usually have an anteroposterior diameter near 1 : 1.

Abnormal Extremity Findings

The inspection of the patient's extremities should include the following:

•Altered skin color (e.g., cyanotic, pale, red, purple, etc.)

•Presence or absence of digital clubbing

•Presence or absence of peripheral edema

•Presence or absence of distended neck veins

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Altered Skin Color

A general observation of the patient's skin color should be routinely performed. For example, does the patient's skin color appear normal—pink, tan, brown, or black? Is the skin cold or clammy? Does the skin and/or mucous membranes appear ashen or pallid? This appearance could be caused by anemia or acute blood loss. Do the patient's eyes, face, trunk, and arms have a yellow, jaundiced appearance (caused by increased bilirubin in the blood and tissue)? Is there redness of the skin or erythema (often caused by capillary congestion, inflammation, or infection)? Does the patient appear cyanotic?

Cyanosis

Cyanosis is common in severe respiratory disorders. Cyanosis is the term used to describe the blue-gray or purplish discoloration of the mucous membranes, fingertips, and toes whenever the blood in these areas contains at least 5 g/dL of reduced hemoglobin. When the normal 14 to 15 g/dL of hemoglobin is fully saturated, the PaO2 is about 97 to 100 mm Hg

and there is about 20 mL/dL of oxygen in the blood. In a typical cyanotic patient with one-third (5 g/dL) of the hemoglobin reduced, the PaO2 is about 30 mm Hg and there is 13 mL/dL of oxygen in the blood (Fig. 3.22).

FIGURE 3.22 Cyanosis is likely whenever the blood contains at least 5 g/100 mL of reduced hemoglobin (Hb). In the normal individual who has about 15 g of hemoglobin per 100 mL of blood, a PO2 of about 30 mm Hg produces 5 g/100 mL of reduced

hemoglobin. The hemoglobin, however, is still approximately 60% saturated with oxygen.

The detection and interpretation of cyanosis are problematic in clinical practice, and wide individual variations occur among observers. The recognition of cyanosis depends on the acuity of the observer, the light conditions in the examining room, and the pigmentation of the patient. Cyanosis of the nail beds is also influenced by temperature, because vasoconstriction induced by cold (i.e., hypothermia) may slow circulation to the point at which the blood becomes hypoxic (bluish) in the surface capillaries even though the arterial blood in the major vessels is not lacking in oxygen.

Central cyanosis, as observed on the mucous membranes of the lips and mouth, is almost always a sign of severe hypoxemia and therefore has definite diagnostic value.

In the patient with polycythemia, cyanosis may be present at a PaO2 well above 30 mm Hg because the amount of

reduced hemoglobin is often greater than 5 g/dL in these patients, even when their total oxygen content is within normal limits. In respiratory disease, cyanosis is the result of (1) a decreased V/Q, (2) pulmonary shunting, (3) venous admixture, and (4) hypoxemia.

Digital Clubbing

Digital clubbing is sometimes observed in patients with chronic respiratory disorders. Clubbing is characterized by a bulbous swelling of the terminal phalanges of the fingers and toes. The contour of the nail becomes rounded both longitudinally and transversely, which results in an increase in the angle between the surface of the nail and the dorsal surface of the terminal phalanx (Fig. 3.23).

FIGURE 3.23 Digital clubbing and cyanosis.

The specific cause of clubbing is unknown. It is a normal hereditary finding in some families without any known history of cardiopulmonary disease. It is believed that the following factors may be causative: (1) circulating vasodilators, such as bradykinin and the prostaglandins, that are released from normal tissues but are not degraded by the lungs because of intrapulmonary shunting, (2) chronic infection, (3) unspecified toxins, (4) capillary stasis from increased venous back pressure, (5) arterial hypoxemia, and (6) local hypoxia. Successful treatment of the underlying disease may result in at least some resolution of the clubbing and return of the digits to normal.

Peripheral Edema

Bilateral, dependent pitting edema is commonly seen in patients with congestive heart failure, cor pulmonale, and hepatic cirrhosis. To assess the presence and severity of pitting peripheral edema, the health care practitioner places a finger or fingers over the tibia or medial malleolus (2 to 4 inches above the foot), firmly depresses the skin for 5 seconds, and then releases. Normally, this procedure leaves no indentation, although a pit may be seen if the person has been standing all day or is pregnant. If pitting is present, it is graded on the following subjective scale: 1+ (mild, slight depression) to 4+ (severe, deep depression) (Fig. 3.24).

FIGURE 3.24 4+ pitting edema. (From Bloom, A., & Ireland, J. [1992]. Color atlas of diabetes [2nd ed.]. London: Mosby-Wolfe.)

Distended Neck Veins and Jugular Venous Distention

In patients with left-heart failure (congestive heart failure), right-heart failure (cor pulmonale), severe flail chest, pneumothorax, or pleural effusion, flow from the major veins of the chest that return blood to the right side of the heart may be compromised. When this happens, cardiac venous return decreases and central venous pressure increases. This condition is manifested by distended neck veins also called jugular venous distention (Fig. 3.25). The reduced venous return also may cause the patient's cardiac output and systemic blood pressure to decrease. In severe cases, the veins over the entire upper anterior thorax may be dilated.

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FIGURE 3.25 Distended neck veins (arrows). Prominence of sternocleidomastoid muscle is also seen in the lower portion of this photograph.

Normal and Abnormal Sputum Production

Normal Histology and Mucus Production of the Tracheobronchial Tree

The wall of the tracheobronchial tree is composed of three major layers: an epithelial lining, the lamina propria, and a cartilaginous layer (Fig. 3.26).

FIGURE 3.26 The Normal Lung. ALV, Alveoli; BM, Basement Membrane; BR, Bronchioles; C, Cartilage; EP, Epithelium; GC, Goblet Cell; LP, Lamina Propria; MC, Mast Cell; PA, Pulmonary Artery; PN, Parasympathetic Nerve; RB, Respiratory Bronchioles; SG, Submucosal Gland; SM, Smooth Muscle; TBR, Terminal Bronchioles.

The epithelial lining, which is separated from the lamina propria by a basement membrane, is predominantly composed of pseudostratified, ciliated, columnar epithelium interspersed with numerous mucus-secreting glands and serous cells. The ciliated cells extend from the beginning of the trachea to—and sometimes including—the respiratory bronchioles. As the tracheobronchial tree becomes progressively smaller, the columnar structure of the ciliated cells gradually decreases

in height. In the terminal bronchioles, the epithelium appears more cuboidal than columnar. These cells flatten even more in the respiratory bronchioles (see Fig. 3.26).

A mucous layer, commonly referred to as the mucous blanket, covers the epithelial lining of the tracheobronchial tree (Fig. 3.27). The viscosity of the mucous layer progressively increases from the epithelial lining to the inner luminal surface and has two distinct layers: the sol layer, which is adjacent to the epithelial lining, and the gel layer, which is the more viscous layer adjacent to the inner luminal surface. The mucous blanket is 95% water. The remaining 5% consists of glycoproteins, carbohydrates, lipids, DNA, some cellular debris, and foreign particles.

FIGURE 3.27 The epithelial lining of the tracheobronchial tree insert drawing shows cilia beating and propelling mucus toward the mouth.

The mucous blanket is produced by the goblet cells and the submucosal, or bronchial, glands. The goblet cells are located intermittently between the pseudostratified, ciliated columnar cells distal to the terminal bronchioles.

Most of the mucous blanket is produced by the submucosal glands, which extend deeply into the lamina propria and are composed of different cell types: serous cells, mucous cells, collecting duct cells, mast cells, myoepithelial cells, and clear cells, which are probably lymphocytes. The submucosal glands are particularly numerous in the medium-sized bronchi and disappear in the bronchioles. These glands are innervated by parasympathetic (cholinergic) nerve fibers and normally produce about 100 mL of clear, thin bronchial secretions per day.

The mucous blanket is an important cleansing mechanism of the tracheobronchial tree. Inhaled particles stick to the mucus. The distal ends of the cilia continually strike the innermost portion of the gel layer and propel the mucous layer, along with any foreign particles, toward the larynx. At this point, the cough mechanism moves secretions beyond the larynx and into the oropharynx. This mucociliary mechanism is commonly referred to as the mucociliary transport or the mucociliary escalator. The cilia move the mucous blanket at an estimated average rate of 2 cm/min. Fig. 3.28A and B shows a microscopic view of normal and abnormal (caused by chronic smoking) pseudostratified columnar ciliated epithelium.

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FIGURE 3.28 Normal pseudostratified columnar ciliated epithelium (A) is contrasted with that of a patient with chronic bronchitis secondary to years of smoking (B). Note the marked thickening of the mucous gland layer (approximately twice normal) and the squamous metaplasia of lung epithelium. (A, Courtesy Mr. Peter Helliwell and the late Dr. Joseph Mathew, Department of Histopathology, Royal

Cornwall Hospitals Trust, UK. In Standring, S. [2016]. Gray's anatomy: The anatomical basis of clinical practice [41st ed.]. London: Elsevier. B, From the Teaching Collection of the Department of Pathology, University of Texas, Southwestern Medical School, Dallas, TX. In Kumar, V. K., Abbas, A. K., & Aster, J. C. [2018]. Robbins basic pathology [10th ed.]. Philadelphia, PA: Elsevier.)

The submucosal layer of the tracheobronchial tree is the lamina propria. Within the lamina propria is a loose, fibrous tissue that contains tiny blood vessels, lymphatic vessels, and branches of the vagus nerve. A circular layer of smooth muscle is also found within the lamina propria. It extends from the trachea down to and including the terminal bronchioles.

The cartilaginous structures that surround the tracheobronchial tree progressively diminish in size as the airways extend into the lungs. The cartilaginous layer is completely absent in bronchioles less than 1 mm in diameter. Fig. 3.29 shows a cross-sectional view of cartilaginous central airway.

FIGURE 3.29 Cross-sectional view of normal cartilaginous central airway. C, Cartilage; E, epithelial surface; G, submucous gland; L, lumen; M, smooth muscle. Mucus in the lumen does not stain well without special stain preparations. (From

Kierszenbaum, A. L., & Tres, L. L. [2016]. Histology and cell biology: An introduction to pathology [4th ed.]. Philadelphia, PA: Elsevier.)

Abnormal Sputum Production

Excessive sputum production is commonly seen in respiratory diseases that cause an acute or chronic inflammation of the tracheobronchial tree. Sputum volume, appearance, viscosity, and odor should be part of the objective finding in a good SOAP note (see Chapter 12, Recording Skills and Intraprofessional Communication). Depending on the severity and nature of the respiratory disease, sputum production may take several forms. For example, during the early stages of tracheobronchial inflammation, the sputum is usually clear, thin, and odorless. As the disease intensifies, the sputum becomes yellow-green and opaque, signifying the early stages of infection. The yellow-green appearance results from an enzyme (myeloperoxidase) released during the cellular breakdown of leukocytes. It also may be caused by retained or stagnant secretions or secretions caused by an acute infection.

Thick and tenacious sputum is commonly seen in patients with chronic bronchitis, chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis, and asthma. Patients with pulmonary edema expectorate a thin, frothy, pinkish sputum. Technically, this fluid is not true sputum. It results from the movement of plasma and red blood cells across the alveolar-capillary membrane into the alveoli.

Hemoptysis

Hemoptysis is the coughing up of blood or blood-tinged sputum from the tracheobronchial tree. In true hemoptysis the sputum is usually bright red and interspersed with air bubbles.

Clinically, hemoptysis may be confused with hematemesis, which is blood that originates from the upper gastrointestinal tract and usually has a dark, coffee-ground appearance. Repeated expectoration of blood-streaked sputum is seen in chronic bronchitis, bronchiectasis, cystic fibrosis, pulmonary embolism, lung cancer, necrotizing infections, tuberculosis, and fungal diseases. A small amount of hemoptysis is common after bronchoscopy, particularly when biopsies are performed. Massive hemoptysis is defined as coughing up 400 to 600 mL of blood within a 24-hour period. Death from exsanguination resulting from hemoptysis is rare. Table 3.4 provides a general overview and analysis of the types of sputum commonly seen in the clinical setting. Fig. 3.30 is a sputum color chart. Although there is considerable interrater reliability in judging color, its use in recording and charting may be helpful.

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TABLE 3.4

Analysis of Sputum Color and Characteristics

Color and Characteristics	Indications and Conditions
Brown/dark	Old blood
Bright red (hemoptysis)	Fresh blood (bleeding tumor, tuberculosis)
Clear and translucent	Normal
Copious	Large amount
Frank hemoptysis	Massive amount of blood
Green	Stagnant sputum or gram-negative bacteria
Green and foul smelling	Pseudomonas or anaerobic infection
Mucoid (white/gray)	Asthma, chronic bronchitis
Pink, frothy	Pulmonary edema
Tenacious	Secretions that are sticky or adhesive or otherwise tend to hold together
Viscous	Thick, sticky, or glutinous
Yellow or opaque	Presence of white blood cells, bacterial infection

FIGURE 3.30 Illustration of a sputum color chart. Samples C and H strongly suggest a diagnosis of hemoptysis. Samples E and G may well be only saliva. (Modified from Reychler, G., et al. [2016]. Reproducibility of the sputum color evaluation depends on the category of

caregivers. Respiratory Care. 61, 7, 936-942.)

Cough

A cough is a sudden, audible expulsion of air from the lungs. It is commonly seen in respiratory disease, especially in disorders that cause inflammation of the tracheobronchial tree. In general, a cough is preceded by (1) a deep inspiration,

(2) partial closure of the glottis, and (3) forceful contraction of the accessory muscles of expiration to expel air from the lungs. In essence, a cough is a protective mechanism that clears the lungs, bronchi, or trachea of irritants. A cough also prevents the aspiration of foreign material into the lungs. For example, a cough is a common symptom associated with chronic sinusitis and postnasal drip. The effectiveness of a cough depends largely on the depth of the preceding inspiration and the extent of dynamic compression of the airways.

Although a cough may be voluntary, it is usually a reflex response that arises when an irritant stimulates the irritant receptors (also called subepithelial mechanoreceptors). The irritant receptors are located in the pharynx, larynx, trachea, and large bronchi. When stimulated, the irritant receptors send a signal by way of the glossopharyngeal nerve (cranial nerve IX) and vagus nerve (cranial nerve X) to the cough reflex center located in the medulla. The medulla then causes the glottis to close and the accessory muscles of expiration to contract. Box 3.4 lists common factors that stimulate the irritant receptors.

Box 3.4

Common Factors That Stimulate the Irritant Receptors

•Inflammation

•Infectious agents

•Excessive secretions

•Noxious gases (e.g., cigarette smoke, chemical inhalation)

•Very hot or very cold air

•A mass of any sort obstructing the airway or compressing the lungs

•Mechanical stimulation (e.g., endotracheal suctioning, compression of the airways)

Clinically, a cough is termed productive if sputum is produced and nonproductive (<25 mL/24 hr) if no sputum is produced.

Nonproductive Cough

Common causes of a nonproductive cough include (1) irritation of the airway, (2) inflammation of the airways, (3) mucous accumulation, (4) tumors, and (5) irritation of the pleura.

Productive Cough

For a productive cough, the respiratory practitioner should assess the following:

•Is the cough strong or weak? In other words, does the patient have a good or poor ability to mobilize bronchial secretions? A good, strong cough may indicate only deep breathing and cough therapy, whereas an inadequate cough may suggest the need for chest physical therapy or postural drainage.

•A productive cough should be evaluated in terms of its frequency, pitch, and loudness. A brassy cough may indicate a tumor, whereas a barking or hoarse cough indicates croup.

•Finally, the sputum of a productive cough should be monitored and evaluated frequently in terms of amount (teaspoons, tablespoons, cups), consistency (thin, thick, tenacious), odor, and color (see Table 3.4).

Self-Assessment Questions

1.An individual's ventilatory pattern is composed of which of the following?

1.Inspiratory and expiratory force

2.Ventilatory rate

3.Tidal volume

4.Inspiratory and expiratory ratio

a.1 and 3 only

b.2 and 3 only

c.2, 3, and 4 only

d.1, 2, and 3 only

2.What is the average total compliance of the lungs and chest wall combined?

a.0.05 L/cm H2O

b.0.1 L/cm H2O

c.0.2 L/cm H2O

d.0.3 L/cm H2O

3.When lung compliance decreases, which of the following is seen?

1.Ventilatory rate usually decreases.

2.Tidal volume usually decreases.

3.Ventilatory rate usually increases.

4.Tidal volume usually increases.

a.1 only

b.2 only

c.3 and 4 only

d.2 and 3 only

4.What is the normal airway resistance in the tracheobronchial tree?

a.0.5 to 1.0 cm H2O/L/s

b.1.0 to 2.0 cm H2O/L/s

c.2.0 to 3.0 cm H2O/L/s

d.3.0 to 4.0 cm H2O/L/s

5.When the systemic blood pressure increases, the aortic and carotid sinus baroreceptors initiate reflexes that cause which of the following?

1.Increased heart rate

2.Decreased ventilatory rate

3.Increased ventilatory rate

4.Decreased heart rate

a.1 only

b.2 only

c.3 only

d.2 and 4 only

6.What is the anteroposterior-transverse chest diameter ratio in the normal adult?

a.1 : 0.5

b.1 : 1

c.1 : 2

d.1 : 3

e.1 : 4

7.Which of the following muscles originate from the clavicle?

1.Scalene muscles

2.Sternocleidomastoid muscles

3.Pectoralis major muscles

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4. Trapezius muscles

a.1 only

b.2 only

c.4 only

d.2 and 3 only

8.Which of the following is associated with digital clubbing? 1. Chronic infection

2.Local hypoxia

3.Circulating vasodilators

4.Arterial hypoxemia

a.2 only

b.2 and 4 only

c.2, 3, and 4 only

d.1, 2, 3, and 4

9.Which of the following is associated with pleuritic chest pain? 1. Lung cancer

2.Pneumonia

3.Myocardial ischemia

4.Tuberculosis

a.1 only

b.2 only

c.1 and 3 only

d.1, 2, and 4 only