5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

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7.Define the following components of a SOAP progress note and list one or more examples.

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8.According to the Respiratory Care Protocol guide (see Fig. 12.2), what are the three major indicators (assessments) for mechanical ventilation?

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9.A patient arterial blood gas values reveal pH of 7.56, PaCO2 of 24, of 20, and PaO2 of 52. Based on the blood gas values, identify the indication(s) for initiation of mechanical ventilation.

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10.Case: A 36-year-old woman is in the emergency department in respiratory distress. Her heart rate is 136 beats/min, and her blood pressure is 165/120 mm Hg. Her

respiratory rate is 32 breaths/min, and her breathing is labored. The patient states that “It feels like a rope is around my neck.” Expiratory wheezing and rhonchi are

auscultated bilaterally. Her arterial blood gas values reveal a pH of 7.56, a PaCO2 of 28, of 21, and a PaO2 of 47 (on room air). Her cough effort is strong, and she is

producing a moderate amount of thin white secretions. Her peak expiratory flow rate is 185 L/min, and her chest x-ray film demonstrates a moderately depressed diaphragm and alveolar hyperinflation.

With this clinical information, provide SOAP documentation for the patient (use Fig. 12.2 for assistance).

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1The authors fully expect that the student will become proficient in the development and automatic use of good “SOAP notes” as a result of reading—and studying—this textbook.

2Thinking in the SOAP format is every bit as important as writing a progress note in it. We hope that instructors who read this chapter will share our enthusiasm when teaching students to present and discuss cases, report at shift change times, justify treatment plan changes, etc.

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Introduction

The Venn diagram shown above illustrates all the possible subsets of patients with chronic bronchitis, emphysema, or asthma (see description of subsets above).

Introduction

Obstructive lung diseases are characterized by a variety of pathologic conditions, such as bronchial inflammation, excessive airway secretions, mucous plugging, bronchospasm, and distal airway weakening, that cause a reduction of air flow into and out of the lungs. Gas flow reduction is especially decreased during exhalation. The most common obstructive lung disorders are chronic bronchitis, emphysema, and asthma.

As shown in the Venn diagram,1 although chronic bronchitis (subset 3), emphysema (subset 4), and asthma (subset 9) may appear alone, they often appear in combination. For example, when chronic bronchitis and emphysema appear together as one disease complex (subset 5), the patient is said to have chronic obstructive pulmonary disease (COPD).

Asthma is represented by subset 9, which by definition is associated with reversible air flow obstruction and therefore is not considered to be COPD. In some cases, however, it is virtually impossible to differentiate patients with partially reversible air flow obstruction from the patient with chronic bronchitis or emphysema who has partially reversible air flow obstruction and hyperreactivity. Thus asthma patients with unremitting asthma are classified as having COPD (subsets 6, 7, and 8).

Chronic bronchitis and emphysema with air flow obstruction are commonly seen together (subset 5 and called COPD), and some patients also may have asthma associated with these two disorders (subset 8). Patients with asthma exposed to chronic irritation, such as from cigarette smoke, may develop a chronic productive cough, a feature associated with chronic bronchitis (subset 6). Such patients are said to have asthmatic bronchitis, or the asthmatic form of COPD. Patients with chronic bronchitis and/or emphysema, without air flow obstruction are not classified as having COPD (subsets 1, 2, and 11). The patient demonstrating overlapping signs and symptoms of both asthma and emphysema (subset 7) is discussed on page 228.

Finally, other obstructive lung disorders include cystic fibrosis and bronchiectasis (less common) and are not generally included in this definition (subset 10).

1A Venn diagram, or set diagram, is a diagram that shows all possible logical relations among a finite collection of sets (aggregation of things). The Venn diagrams were first conceived around 1880 by John Venn. They are used to teach elementary set theory and illustrate simple set relationships in probability, logic, statistics, linguistics, and computer science.

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Centriacinar Emphysema

Centrilobular Emphysema Chronic Bronchitis

Chronic Obstructive Pulmonary Disease (COPD) COPD Assessment Test (CAT)

Endobronchial One-Way Valves or Lung Coils End-of-Life Care (Palliative) Care Emphysema

Global Initiative for Chronic Obstructive Lung Disease (GOLD) Hoover sign

Lung Transplantation

Lung Volume Reduction Surgery (LVRS) MM Alpha1-Antitrypsin Phenotype

Modified British Medical Research Council (mMRC) Breathlessness Scale MZ Alpha1-Antitrypsin Phenotype

Panacinar Emphysema

Panlobular Emphysema “Pink Puffer”

Pulmonary Rehabilitation Spirometry Test

ZZ Alpha1-Antitrypsin Phenotype

The American Thoracic Society (ATS) guidelines for chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema provide the following definitions:

Chronic obstructive pulmonary disease is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive, is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, and is primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.

Chronic bronchitis is defined clinically as chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded.

Emphysema is defined pathologically as the presence of permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of bronchiole walls and without obvious fibrosis.

In patients with COPD, both chronic bronchitis and emphysema are present. However, the relative contribution of each to the disease process is often difficult to discern. Note that the ATS definition for chronic bronchitis is based on the major clinical manifestation associated with the disease (i.e., productive cough). Also note that the ATS definition for emphysema is based on the pathologic findings or the anatomic alterations of the lung associated with the disorder.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) now provides the following working definition1:

Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is caused by airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

Note that the GOLD definition does not use the terms chronic bronchitis and emphysema. GOLD explains that emphysema, or destruction of the gas-exchanging surfaces of the lung (alveoli), is a pathologic (i.e., anatomic alteration of the lung) term that is often—but incorrectly—used clinically and describes only one of the several structural abnormalities present in the patient with COPD. Chronic bronchitis, or the presence of cough and sputum production (i.e., clinical manifestations) for at least 3 months in each of 2 consecutive years, remains a clinically and epidemiologically useful term but is present in only a minority of subjects when this definition is used.

The bottom line is this: even though chronic bronchitis and emphysema can each develop alone, they often occur together as one disease entity. When this happens, the disease entity is called chronic obstructive pulmonary disease (COPD). In other words, COPD is a term referring to two lung diseases—chronic bronchitis and emphysema—occurring simultaneously. Patients with COPD demonstrate a variety of clinical manifestations associated with both disorders, although the relative contribution of each respiratory disorder is often difficult to ascertain. For this reason, chronic bronchitis, emphysema, or a combination of both disorders (COPD) are treated as one disease entity in the clinical setting.2

Anatomic Alterations of the Lungs Associated With Chronic Bronchitis

The conducting airways (particularly the bronchi) are the primary structures that undergo change in chronic bronchitis. As a result of chronic inflammation, the bronchial walls are narrowed by vasodilation, congestion, and mucosal edema. This condition is often accompanied by bronchial smooth muscle constriction. In addition, continued bronchial irritation causes the submucosal bronchial glands to enlarge and the number of goblet cells to increase, resulting in excessive mucous production. The number and function of cilia lining the tracheobronchial tree are diminished, and the peripheral bronchi are often partially or totally occluded by inflammation and mucous plugs, which in turn leads to hyperinflated alveoli (Fig. 13.1). Fig. 13.2 shows two microscopic views of chronic bronchitis.

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FIGURE 13.1 Chronic bronchitis, one of the most common airway diseases. SMC, Smooth muscle constriction; ESG, enlarged submucosal gland; HALV, hyperinflation of alveoli (distal to airway obstruction); IEP, inflammation of epithelium; MA, mucous accumulation; MP, mucous plug.

(A) Chronic bronchitis, microscopic. This bronchus (lower right corner) has increased numbers of chronic inflammatory cells (arrows) in the submucosal bronchial region. (B) Chronic bronchitis. The lumen of the bronchus is above. Note the marked thickening of the mucous gland layer (approximately twice normal) and squamous metaplasia of lung epithelium. (A, From Klatt, E. C. [2015]. Robbins and Cotran Atlas of Pathology [3rd ed.]. Philadelphia, PA: Elsevier. B, From the Teaching Collection of

the Department of Pathology, University of Texas, Southwestern Medical School, Dallas, Texas. In Kumar, V., Abbas, A. K., Aster, J. C. [2018]. Robbins Basic Pathology [10th ed.]. Philadelphia, PA: Elsevier.)

To summarize, the following major pathologic or structural changes are associated with chronic bronchitis:

•Chronic inflammation and thickening of the walls of the peripheral airways.

•Excessive mucous production and accumulation.

•Partial or total mucous plugging of the airways.

•Smooth muscle constriction of bronchial airways (bronchospasm)—a variable finding.

•Air trapping and hyperinflation of alveoli may occur in late stages.

Anatomic Alterations of the Lungs Associated With Emphysema

Emphysema is characterized by a weakening and permanent enlargement of the air spaces distal to the terminal bronchioles and by destruction of the alveolar walls. As these structures enlarge and the alveoli coalesce, many of the adjacent pulmonary capillaries also are affected, resulting in a decreased surface area for gas exchange across the alveolar-capillary membrane. Furthermore, the distal airways, weakened in the process, tend to collapse during expiration in response to increased intrapleural pressure. This traps gas in the alveoli. There are two major types of emphysema: panacinar (panlobular) emphysema and centriacinar (centrilobular) emphysema.

In panacinar emphysema, or panlobular emphysema, there are an abnormal weakening and enlargement of all alveoli distal to the terminal bronchioles, including the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli; the entire acinus is affected by dilatation and destruction. The alveolar-capillary surface area is significantly decreased (Fig. 13.3). Panlobular emphysema is commonly found in the lower parts of the lungs and is sometimes associated with a deficiency of the protease inhibitor alpha1-antitrypsin. Panlobular emphysema is one of the more severe types of

emphysema and therefore the most likely to produce significant clinical manifestations.

In centriacinar emphysema, or centrilobular emphysema, the pathologic issues involve the respiratory bronchioles in the proximal (central) portion of the acinus. The respiratory bronchiolar walls enlarge, become confluent, and are then destroyed. A rim of parenchyma remains relatively unaffected (Fig. 13.4). Centriacinar emphysema is the most common form of emphysema and is strongly associated with cigarette smoking and with chronic bronchitis. Fig. 13.5 shows a microscopic view of pulmonary emphysema.

FIGURE 13.4 Centrilobular emphysema. Abnormal weakening and enlargement of the respiratory bronchioles and alveoli in the proximal portion of the acinus.

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FIGURE 13.3 Panlobular emphysema. (A) Normal alveoli for comparison purposes. (B) Panlobular emphysema. Abnormal weakening and enlargement of all air spaces distal to the terminal bronchioles.

The normal level of alpha1-antitrypsin ranges between 150 and 350 mg/dL (1.5 to 3.5 g/L) when measured via radial immunodiffusion. Patients with normal levels of alpha1-antitrypsin are referred to genetically as having an MM alpha1-antitrypsin phenotype or simply an M

phenotype (homozygote). The phenotype associated with severely low serum concentrations is the ZZ alpha1-antitrypsin phenotype, or simply Z. The heterozygous offspring of parents

with the M and Z phenotypes have an MZ alpha1-antitrypsin phenotype. The MZ alpha1- antitrypsin phenotype results in an intermediate deficiency of alpha1-antitrypsin. The precise effect of the intermediate level of alpha1-antitrypsin is unclear. It is strongly recommended,

however, that individuals with this phenotype do not smoke or work in areas having significant environmental air pollution. Although alpha1-antitrypsin deficiency is considered to be rare, it

is estimated that 80,000 to 100,000 individuals in the United States have severe deficiency of alpha1-antitrypsin.

•Age and gender: As a person ages, the risk for COPD increases. Although the precise connection between age and COPD is unclear, it is suggested it may be related to the sum of cumulative exposures throughout life. In the past, COPD was greater among men than women. However, more recent data indicate that the prevalence of COPD between men and women is about equal, likely reflecting the changing patterns of tobacco smoking.

•Lung growth and development: Any condition that affects lung growth during gestation and childhood (e.g., low birth weight, respiratory infections) has the potential for increasing an individual's risk for developing COPD (see Chapter 33, The Newborn Disorders).

•Exposure to particles

•Tobacco smoke: Cigarette smoking is the most commonly encountered risk factor for COPD worldwide. Other types of tobacco (e.g., pipe, cigar, water pipe) and marijuana are also risk factors for COPD. Passive exposure to cigarette smoke also may cause COPD. Smoking during pregnancy may affect lung growth and development of the fetus.

•Occupational exposure: Organic and inorganic dusts and chemical agents and fumes (e.g., asbestos, coal dust, moldy hay, bird droppings, or paints) may cause COPD.

•Indoor air pollution: Wood, animal dander and dung, crop residues, and coal, commonly burned in open fires or poorly functioning stoves, may lead to very high levels of indoor pollution. Research data continue to grow that indoor pollution from biomass in cooking and heating3 in poorly ventilated areas is an important risk factor for COPD. It is estimated that about 3 billion people around the world use biomass and coal as their primary source of energy for cooking, heating, and basic household needs.

•Outdoor air pollution: Although high levels of air pollution (e.g., silicates, sulfur dioxide, the nitrogen oxides, and ozone) are known to be harmful to individuals with existing heart and lung disease, the role of outdoor pollution in causing COPD is unclear.

•Socioeconomic status: Poverty is clearly a risk factor for COPD, although the precise components associated with poverty and COPD are unclear. Likely factors include exposure to indoor and outdoor air pollutants, crowding, poor nutrition, and infection. The data strongly suggest that the risk for developing COPD is inversely related to an individual's socioeconomic status.

•Asthma/bronchial hyperreactivity: Asthma may be a risk factor for the development of COPD.

•Chronic bronchitis: May be a risk factor for the development of COPD. In other words,

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