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Chronic Respiratory Conditions (FL INITIAL Autonomous Practice - Pharmacology)

2 Contact Hours including 2 Advanced Pharmacology Hours
Only FL APRN's will receive credit for this course
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This course is only applicable for Florida nurse practitioners who need to meet the autonomous practice initial licensure requirement.
This peer reviewed course is applicable for the following professions:
Advanced Practice Registered Nurse (APRN)
This course will be updated or discontinued on or before Monday, April 14, 2025

Nationally Accredited

CEUFast, Inc. is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. ANCC Provider number #P0274.


≥ 92% of participants will understand the pathology, management, and optimization of chronic respiratory conditions.

Chronic respiratory conditions contribute to the global burden of diseases. Respiratory conditions, including asthma, chronic obstructive pulmonary disease (COPD), interstitial lung disease, and pulmonary sarcoidosis, are undoubtedly the most common non-communicable disease worldwide. Unfortunately, these conditions have consistently received proportionately less public attention and fewer clinical investigations in the medical community. As it stands, only a handful of research funding is dedicated primarily to studying the global distribution, epidemiology, and new treatment options for chronic respiratory conditions. Recent estimates have revealed a growing trend of primary occurrences and respiratory-linked mortality cases, especially in regions with poor healthcare services. The immediate response to these observations has since facilitated a global resurgence in clinical interest in preventable respiratory conditions. This course is designed to discuss highlights of chronic respiratory diseases as they affect the global population. It also presents a balanced view of the standards of assessment, diagnosis, drug care, supportive management, and nursing roles as it relates to respiratory conditions.


After completing this continuing education course, the participants will be able to meet the following objectives:

  1. Identify the clinical course and pathology of commonly reported chronic respiratory conditions.
  2. Evaluate the acceptable standards and protocols for executing clinical plans in chronic respiratory care as it affects assessment, diagnosis, therapy plan, and documentation.
  3. Analyze the widely accepted standards of primary care for respiratory conditions.
  4. Outline the different standards of medication plans and supportive care regimens.
  5. Summarize general recommendations and therapy modifications linked to improved prognosis in chronic care.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

Last Updated:
To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Jassin Jouria (MD)

Chronic Respiratory Disease as a Global Healthcare Burden

In modern medicine, it is common to find different healthcare awareness programs and patient-centered learning models centered on chronic respiratory conditions in humans. On the global scale, these conditions are considered the leading cause of mortality, morbidity, economic burden, and disability-adjusted life years in many people. Chronic respiratory diseases (CRDs) primarily affect the respiratory system's biological architecture, including the lungs, the pulmonary vasculature, the trachea, and the parenchyma. Over the years, the focus of care on these conditions has shifted rapidly to include the design of optimal treatment and/or prevention plans in addition to different methods to alleviate or control symptomatology. Although the number of conditions that directly falls under the general description of CRDs is quite plenty, asthma, COPD, interstitial lung diseases, lung cancer, and cystic fibrosis are commonly described. Tuberculosis, a major communicable respiratory disease, has also been discussed recently in light of an increasing antibiotic resistance expressed by the bacterial pathogen -Mycobacterium tuberculosis.

Since CRDs primarily attack the biological architecture of the respiratory tracks, understanding the physiology and morphology of the respiratory system better informs of the healthcare burden of CRDs. The respiratory tract is subdivided into two major parts – the upper and lower respiratory tract. The upper respiratory tract consists of the nose, mouth, and the initial portion of the trachea. The lower respiratory tract, on the other hand, is composed of the bronchioles, the later part of the trachea that progressively terminates into the bronchi, and the functional respiratory units known as the alveoli. Functionally, the complete processes of gas exchange occur with the support of the pulmonary vasculature as the airways derive consistent support from the lung parenchyma (Mikolasch et al., 2022). An essential function of the respiratory system is the exchange of gases – a process described exclusively as the intake of oxygen (O2) and the disposal of carbon dioxide (CO2). The single membranes of the pulmonary alveolus assume a significant role in this process as the exchange of gases occurs in their thin films.

The process of breathing includes inhalation, that is, the primary expansion of chest volume for the intake of air. The inhaled air then moves through the smaller "conductive" airways, and exhalation occurs. Exhalation is the release of air from the lungs as the chest volumes progressively contract. Two main muscle types facilitate the breathing process – the diaphragm and intercostal muscles. (Thomen et al., 2020). On average, the weight of a normal human lung is estimated at 1 kg, with around half (40%–50%) of that volume attributed to blood in the pulmonary vasculature. To establish the presence of obstructive lung diseases or a progressive lung impairment, conducting a measurement of the volume and action of breathing is important; this principle is essential in diagnosing lung diseases like asthma and COPD.

The complete path of pulmonary mechanics includes the efficient exchange of gas and requires biological input from the multiple components of the respiratory tract. Although it looks automated, efficient gas exchange depends directly on the consistency and accuracy of different measurements unutilized in monitoring the normal functioning of the lungs. The means and aids for conducting these measurements have been consistently overhauled and improved over the last few decades. In modern medicine, these measurements are conducted using the principles of spirometry. Spirometry is a safe, practical, and reproducible test to determine the ventilatory capacity of the lungs and identify any changing trends in the functionality of the lung concerning air capacity and gas exchange efficiency. Modern spirometers have the added advantage of generating prompt computer-aided feedback to the operator on the quality and repeatability of the test. Results can also include a real-time, reproducible digital flow chart of the flow-volume curve.

Modern spirometry measurements are directly explored in the assessment and care of chronic respiratory conditions, including tidal volume (TV), inspiratory reserve volume (IRV), and residual volume (RV). Other standard lung capacities that are routinely measured are inspiratory capacity (IC), vital capacity (VC), expiratory reserve volume (ERV), functional residual capacity (FRC), and total lung capacity (TLC) (Rocha et al., 2021).

Image showing spirometric test graph

Fig. 1. Example of a spirometry measurement.

To an extent, the value of these measurements depends directly on the healthiness of the lungs and the associated respiratory apparatus. A normal lung has several cell types that have highly specialized functions. The major cell types found in a healthy one include airway epithelial cells, goblet cells, ciliated cells, and Clara cells. Others may include neuroendocrine, basal, and type I and II alveolar cells. In addition, there are immune, stem, and adipose cells in the lungs. In different CRDs, the biological functionalities of one or more of these cells are completely or partially impaired. For instance, research reports have established a link between lung carcinomas and glandular cells in the lung, especially in subjects with multiple risk factors.

In addition, the pathology of respiratory diseases, such as neonatal respiratory failure, interstitial lung disease (ILD), alveolar proteinosis, and other rare lung diseases, seems to have a link with impairments in the secretion of surfactant proteins and lipids. Changes in the pulmonary vasculature, including smooth muscle hypertrophy and intimal hyperplasia, have been linked to severe hypoxic vasoconstriction of the small pulmonary arteries (Dekkers et al., 2021). Changes to the pulmonary architecture greatly impair respiratory function, forcing the basal cells in the airway epithelium to initiate a series of processes that permanently change the airway architecture. The airway's physical barriers and host-environment defense arrangement are important factors in pulmonary inflammation and the subsequent activation of immune cells; this may also be implicated in the complicated process of pulmonary remodeling and repair (Eenjes et al., 2022).

Overview of Chronic Respiratory Conditions


One of the most referenced reviews focused on the epidemiology of chronic respiratory conditions was published in 2020 by the Lancet Respiratory Medicine. In this review, authors leveraged the Global Burden of Diseases, Injuries, and Risk Factor Study (GDB) to estimate the prevalence and associated health burden of CRDs. The review reported that an estimated 545 million people globally had a CRD in 2017 alone.

The estimate corresponded to a noticeable increase of 39.8% since 1990. The high-income super-regions reported the highest prevalence rate of CRDs, while South Asia and sub-Saharan Africa reported the lowest rates. COPD (3.9% global prevalence) and asthma (3.6%) are the most prevalent CRDs. Disparities in prevalence rate were linked with different region-specific factors that affect healthy living, diet, and exposure to harmful environmental triggers and pathogens. Cumulatively, CRDs caused approximately 3.9 million deaths in 2017 – an estimated increase of 18% since 1990. CRDs also accounted for about 1,470 disability-adjusted life-years per 100,000 individuals, an increase of 13.3% since 1990 (GBD, 2020).

In these researched areas, COPD and asthma were the leading causes of CRD mortality worldwide. However, ILD and pulmonary sarcoidosis were second on the list of causes of death in high-income Latin America. These findings are also consistent with accounts from the Caribbean and the regions of Central Europe, Eastern Europe, and Central Asia (Zeng et al., 2022).

Surprisingly, despite the significant increase in the reported estimates of prevalence and healthcare burden index of CRDs between 1990 and 2017, the age-standardized estimates of prevalence, mortality, and disability-adjusted life-years have decreased steadily over the same timeframe. In addition to the difference in prevalence trends, the risk factors identified by this review also seem to differ concerning gender and geographical location.

Smoking reportedly caused the highest proportion of disability linked to CRD in all regions for males. In women, however, the leading risk factors of respiratory impairment vary largely by region. In South Asia and Sub-Saharan Africa, solid fuel use and prolonged airway exposure to pollutants were the main identified risk factors. Exposure to ambient particulate matter is the leading cause of respiratory impairment in East Asia, Southeast Asia, Oceania, North Africa, and Middle East super-regions. Smoking leads to the commonly documented risk factors in other super-regions. Epidemiological studies also confirm that CRDs are common globally and linked with significant morbidity and mortality rates.

However, the provided estimates also emphasize the statistical difficulties of the global distribution of CRD-related health burdens and risk factors by gender (Bai et al., 2022). Researchers asserted that the lower prevalence rates of certain diseases in South Asia and sub-Saharan Africa might be mostly attributable to inadequate or underutilized diagnostic capabilities in healthcare institutions. On the other hand, the lower mortality rate in sub-Saharan Africa compared to other regions may be attributable to differences in the age distribution of the population, which favors the younger generation, among whom communicable disease-related deaths are reported more frequently than deaths from other chronic diseases.

Understanding the Prevalence, Risk Factors, and Management of Selected Chronic Respiratory Diseases

Chronic Obstructive Pulmonary Disease

COPD is an umbrella term for a spectrum of diseases generally characterized by a progressive limitation in airflow that is not entirely reversible. Over the years, the clinical description and symptomatology classification of COPD has continuously changed in the medical community. Nevertheless, the 1995 European Respiratory Society (ERS) consensus on COPD established a benchmark that has withstood significant scrutiny.

The ERS describes COPD as a condition characterized by a persistent reduction in maximum expiratory flow and slower emptying of the lungs (ERS, n.d.). The majority of airflow restriction is slow-progressing and irreversible. Both airway disease and emphysema contribute to airflow restriction. In many cases, it is difficult to determine in vivo the relative contribution of these two components to COPD pathophysiology. The American Thoracic Society (ATS) has defined COPD as a disease characterized by airflow obstruction predominantly due to chronic bronchitis or emphysema (ATS, 2019). In this instance, the airflow restriction is progressive and may be linked with airway hyper-reactivity, with partially reversible symptoms.

COPD cases reportedly increased by 49.8% from 199,879 in 1990 to 299,398 in 2017. The age-standard incidence rate (ASIR) in females was slightly higher than in males in 1990 and 2017. The rate varied greatly from 90 per 100,000 to 503.1 per 100,000 globally. Papua New Guinea, North Korea, and Lesotho had the highest ASIRs. The least reported ASIRs were from Cape Verde, Singapore, and Japan. Between 1990 and 2017, the ASIR reported a decrease of 0.68% on average in both sexes across the globe. Statistically noticeable reductions in the ASIRs were reported in the Maldives, Singapore, and Thailand. On the other hand, Argentina, Uruguay, and Canada observed the most significant jumps in ASIR value during the study period. However, by 2019, COPD had already afflicted an estimated 212.33 million adults, according to reports published by the Global Burden of Disease Figures (GBD, 2017).

Etiology and Causal Factors of COPD in the General Population

Genetic Determinants

The clinical arguments faulting a genetic component in the development of COPD in premature infants and adults have only waxed stronger over the years. Recently, epidemiologic studies investigating a possible link between etiology and symptomatic presentation have reported that only a meager (10% - 20%) of smokers present with a significantly high risk of developing COPD. Logically, this observation suggests a strong role in genetic susceptibility. Due to the complexities of COPD, the genetic determinants of the condition are expected to be complex in evaluation. A comprehensive investigation identified many candidate genes as factors implicated in COPD pathology. These include the α-1-antitrypsin (AAT) gene, α-1-quimitrypsine genes, α-2-macroglobulin genes, the vitamin D coupling protein, and the blood-serotype group genes. Although animal model experiments evaluating the specific roles of these candidate genes have received huge attention, only α-1-antitrypsin has been linked to COPD development.

Research reports described the AAT gene as highly polymorphic, with a diverse allele count greater than 75. The more common allele variants include the alleles M, S, and Z, with occurrence frequencies of about 0.93, 0.05, and 0.02, respectively. Almost all subjects affected by a severe impairment of the AAT are homozygous for the Z allele. Although there is a strong link between COPD and the AAT gene, only an estimated 1% of COPD cases have been attributed to this gene. The general population has a significantly low prevalence of the relevant AAT gene variants, and other gene candidates appear to contribute to developing more COPD cases than AAT (Crapo et al., 2021).

Phenotypic Susceptibility, including Atopy, Sex, and Bronchial Hyperresponsiveness

Bronchial reactivity and atopy are potential effect modifiers of COPD risk in animal models and clinical findings in humans. The findings of these evaluations imply that hyperresponsive individuals have reduced lung function at some point in their lifespan; however, there are numerous disagreements in this regard. Numerous researchers have observed that bronchial hyperresponsiveness is associated with progressive lung function decline. Others have argued that bronchial responsiveness may be associated with smoking-induced airway inflammation rather than any direct source of lung injury. In addition, the probabilities for bronchial responsiveness among incident cases of chronic cough and phlegm, after correcting for age, sex, region, and smoking, were approximately double the equivalent odds in those who were free of these symptoms until the conclusion of medical follow-up (Wang et al., 2020). After eliminating asthmatic participants from the analysis, those with bronchial reactivity had a decreased risk of symptom remission. The relevance of these findings to COPD is confirmed by a subsequent study demonstrating that COPD mortality increased with increasing bronchial hyperresponsiveness (Proboszcz et al., 2021).

Active and Passive Smoking

Judging from the accumulated studies on the etiology of COPD, active smoking is considered the single most significant cause of COPD, even though epidemiological studies have identified COPD in only a low proportion of heavy smokers. Following the natural history of COPD, the first question is to what extent smoking is a cause of progressive airway dysfunction and loss of active gas exchange properties.

The available literature suggests that smokers have a higher tendency to develop decreased forced expiratory volume (FEV1) both in cross-sectional and longitudinal studies, with the decline in FEV1 pegged at between 7 mL/yr to 33 mL/yr (Chang et al., 2021). There also seems to be a dose-dependent relationship between chronic smoking behavior and the progressive decline in FEV1. Concerning whether smoking cessation might reverse the progression of COPD, the existing research indicates that the FEV1 levels off following smoking cessation but does not return to its baseline level. Multiple studies demonstrate that maternal smoking is associated with a statistically significant reduction in FEV1 and other spirometry parameters in school-aged children in early life (Bitan et al., 2022). A highly cited research article, the Six Cities Study, demonstrated a substantial association between exposure to ambient tobacco smoke and a minor but steady fall in FEV1 volume (−3.8 mL/yr).


Some occupational situations may influence the risk of developing COPD. Occupational risk factors for COPD vary and are likely to be less significant than the effects of smoking and hereditary susceptibility.

Multiple exposures in specific occupations have been evaluated as a significant COPD risk in industry-based research. In this context, exposures to isocyanates, asbestos, silicon, cadmium, coal, and other mineral dust and gases have been examined. Studies based on population clusters provide a detailed report on the association between specific vocations and COPD. According to a corresponding European Community Respiratory Health Society (ECRHS) study in the young general population, continued exposure to high levels of these materials has been linked to a lower progressive decline in FEV1 in Spain. Although this association was only proven for population clusters in the ECHRS participating countries, this is true to a major extent in the global population (Zhang et al., 2021). In multiple longitudinal studies investigating the link between occupation and COPD development, researchers found that occupations with a calculated higher risk of nonspecific chronic lung impairment include wood and paper workers, tailors, construction, and transport workers. People continuously exposed to heavy metals, mineral dust, and adhesives appear to have the most significant risk index. The evidence of occupational risk seems to have an intricate link with socioeconomic status. Early population-based studies found that subjects with primary and secondary education had a higher prevalence of spirometric airflow limitation when compared to subjects with a university education with statistical adjustments for age, sex, and smoking. (Zhang et al., 2021).

Clinical Evaluation and Symptomatology of COPD

A diagnosis of COPD is usually established in chronic smokers within the 40 – 50 age range. However, before a clinical diagnosis is confirmed, a long course of functional and structural changes to the lung must have occurred. Biological changes and other pathologies that lead to progressive decline in lung function, the onset of airway limitation, worsening of health-related life quality, and, frequently, mortality due to COPD are possible. Generally, typical cases of COPD are characterized by a progressive decline in lung function. An important observation at the earliest stage of COPD may involve a biological dysfunction in the development of lung function during early-life stages and adulthood. Combined with a slightly accelerated decline at a later age may precipitate significant limitations in airflow. In many population-based studies, healthy subjects' lung function achieves its maximum value at age 20–25, followed by a slow progressive decline as age increases. Smokers have sharper rates of decline followed by a system-wide development of respiratory symptoms and severe airway obstruction.

Patients with COPD typically have symptoms consistent with increasing and chronic cough, dyspnea, and sputum production. Additionally, wheezing and chest discomfort may be consistently reported across a population (Agarwal et al., 2022). While a smoking history is evident in most cases, many do not have one. It is advised that clinicians evaluate the probabilities and dangers of secondhand smoke exposure, environmental and occupational exposures, and family history. Subjects with a confirmed diagnosis of COPD should be questioned regarding probable exacerbation histories, nightly awakenings, inhaler usage patterns, and the impact of airway impairment on everyday life. Patients may also be questioned about their past medical history for asthma, allergies, and childhood respiratory dysfunctions, among other relevant diseases. In instances with a liver disease consequence, basilar emphysema and emphysema in the family considerably enhance the incidence of α-1 antitrypsin deficiency.

The most documented physical observations in patients with an established case of COPD include the following:

  • Muscle wasting
  • Significant respiratory distress in acute symptomatic exacerbation
  • Wheezing
  • Prolonged expiration
  • Pursed-lip breathing pattern
  • Barrel chest or an increased anterior-posterior chest wall diameter
  • Central cyanosis
  • Lower extremity edema with right-sided heart failure

Spirometry examinations are commonly used to confirm COPD in many subjects. Initial evaluations often involve a 6-minute walk test, laboratory testing, and subsequent radiographic imaging in people presenting with symptoms of airflow limitations and significant risk factor scores for COPD.

Pulmonary function testing (PFT) is essential for diagnosing, staging, and managing COPD (Tsiligianni & Kocks, 2020). Before and after providing control dosages of an inhaled bronchodilator, spirometry is conducted. Inhaled bronchodilators may contain short-acting beta2-agonists (SABA), short-acting anticholinergics, or both. When making a preliminary diagnosis of COPD, experts agree that an FEV1 and forced vital capacity (FVC) ratio of less than 0.7 is diagnostic. Dyspnea-like symptoms in patients with a severely diminished FEV1 should be examined for oxygenation using pulse oximetry or arterial blood gas analysis. The World Health Organization (WHO) and the National Heart, Lung, and Blood Institute launched the Global Initiative for Chronic Obstructive Lung Disease (GOLD) program (NHLBI). The program is globally acclaimed for its comprehensive and up-to-date recommendations for diagnosing and treating COPD. The GOLD recommendations are frequently used to evaluate illness severity and therapeutic selection.

The 2019 edition of these recommendations highlights a procedure for selecting the appropriate treatment plans for patients with a confirmed diagnosis of COPD. The refined airway, breathing, circulation, and disability (ABCD) assessment tool guides clinicians and caregivers to evaluate disease severity and classify presentations based on the GOLD classification. Once the diagnosis of COPD is confirmed by spirometry (FEV1/FVC <0.7), the FEV1 directly help clinicians track disease severity and viable options for symptomatic control, such as with the GOLD classification 1-4).

graphic showing COPD Assessment

Fig. 2. COPD Assessment adapted from GOLD 2020 report.

Clinicians utilize the modified British Medical Research Council questionnaire and the COPD Assessment Test (CAT) to more accurately diagnose patients' disease stages and assess the severity of their symptoms.

The British Medical Research Council questionnaire measures the severity of breathlessness on a scale of 0 to 4. The CAT examines eight functional parameters that directly reflect how the disease impacts the subject's quality of life. In many instances, the COPD evaluation approach for a given patient is contingent upon the disease characteristics and the lung function under direct examination (Singh et al., 2019). Clinicians can further evaluate the submaximal functional capacity of a patient under observation by utilizing a 6-minute walk test. A 6-minute walk test is conducted inside on a flat, straight surface, with the patient walking 100 meters in a straight line. The distance walked during a 6-minute walk is determined.

Clinical Intervention

In the clinical management of COPD, the primary goal of therapy is to improve the quality of life, modify lung function, reduce the risk of symptom exacerbations, and reduce the risk of mortality. Multiple pharmacological approaches with medication use and non-pharmacological approaches – including smoking cessation, have been recommended as clinical interventions in COPD patients. Patients with COPD are generally advised to take an annual influenza vaccination to reduce the risk of comorbidities. In those aged 65 and presenting with a high-risk score, the 13-valent pneumococcal conjugate vaccine (PCV13) and the 23-valent pneumococcal polysaccharide vaccine (PPSV23) are recommended to be taken at least one year apart. The PPSV23 is further advised in those aged 64 and younger presenting with severe comorbidities that can worsen lung impairment. (e.g., diabetes, chronic heart disease, chronic lung disease).

Globally, bronchodilators (beta2-agonists, antimuscarinics, methylxanthines), inhaled corticosteroids (ICS), systemic glucocorticoids, phosphodiesterase-4 (PDE4) inhibitors, and antibiotics are the most commonly prescribed drugs for the treatment of COPD. Beta2-agonists directly relax the smooth muscle of the airways to reduce structural obstructions to airflow, hence enhancing lung function. COPD may also be treated with short-acting beta2-agonists (SABAs) and long-acting beta2-agonists (LABAs). SABAs are administered on a case-by-case basis to ensure quick relief. LABAs are frequently prescribed for maintenance therapy and long-term lung function maintenance. To directly produce bronchoconstriction, antimuscarinics operate on M3 muscarinic receptors in smooth muscle (Shuai et al., 2021). Short-acting antimuscarinic drugs (SAMAs) like SABAs produce quick relief. Long-acting antimuscarinic drugs (LAMAs), like LABAs, are intended primarily for long-term maintenance regimens.

Inhaled corticosteroids are frequently used with LABAs and LAMAs to reduce inflammation in acute and chronic exacerbations. Recent research on combined COPD therapy has demonstrated that combining ICS and LABAs help COPD patients achieve better symptom control than either medicine alone. However, healthcare practitioners should be aware of the increased risk of pneumonia in patients receiving long-term ICS treatment. Oral glucocorticoids are contraindicated for long-term usage and are associated with numerous adverse effects. Instead, these should be retained to treat acute exacerbations (Czira et al., 2022). PDE4 reduces inflammation by decreasing the breakdown of intracellular cyclic adenosine monophosphate (cAMP). Roflumilast is a PDE4 inhibitor that reduces the number of illness exacerbations in people with severe disease. Pulmonary rehabilitation and pharmaceutical treatment are also recommended in all phases of COPD. A complete treatment strategy may include therapies like exercise training, education, and behavior modification. It aims to improve the patient's physical and lung function (Clini & Costi, 2021).


Asthma is a respiratory condition characterized by variable symptoms of wheezing, shortness of breath, chest tightness, and/or cough and by variable worsening of expiratory airflow. The presentation of symptoms and airway impairment that characterize this condition may vary in severity significantly over time. These variations, in many patients, may be exacerbated by factors that include exercise, exposure to allergens, sudden change in weather conditions, or viral respiratory infections. Symptoms and airflow limitation have reportedly resolved due to medication use in many asthmatics. However, in others, these symptoms may be absent for several weeks or months before returning. Presentations of asthma generally vary and depend on the type of asthma and the triggers identified. Some patients may report episodic exacerbations of asthma that may be life-threatening and reduce the quality of life and social living.

Between 1980 and 2014, an estimated 157,066 deaths due to asthma were recorded in the United States alone. The recorded number was significantly higher in countries with poor primary healthcare systems. In 2014 alone, mortality rates secondary to asthma reportedly ranged from 0.5 to 4.1 deaths per 100,000. Based on statistical extrapolations, counties with the highest mortality burden from asthma were located in the southern half of the Mississippi River, Georgia, and South Carolina. Epidemiological research conducted between 1980 and 2014 suggested that mortality rates due to asthma reduced from 46.5% (95% UI, 27.0%-51.8%) to an estimated 1.2 (95% UI, 1.1-1.3) deaths per 100,000.

Simultaneously, the mortality rate was also reduced by a significant 99.6%. Based on the Global Burden of Disease, Injuries, and Risk Factor Study in 2017, the reported number of diagnosed asthma cases reportedly increased from 210,684 in 1990 to an estimated 272,677 in 2017. By 2017, the ASIR of asthma differed considerably worldwide, ranging from 314.1 per 100,000 to 1822.7 per 100,000. Tonga, Puerto Rico, and American Samoa have the three highest reported ASIRs. Similarly, Italy, Spain, and Germany completed the bottom pack of countries with the least reported values of ASIR (Xie et al., 2020).

Asthma contributed to about 69.4% of the total CRD incidence cases observed in 2017 alone. Referencing data collected over the study period, the highest ASIR increases were observed in the Solomon Islands (EAPC = 1.29, 95% UI 1.14–1.44), Pakistan (EAPC =1.00, 95% UI 0.86–1.14), and Samoa (EAPC = 0.98, 95% UI 0.89–1.07). The least ASIR value reductions were reported from South Africa (EAPC = -2.27, 95% UI − 2.92 to − 1.62), Guatemala (EAPC = -1.42, 95% UI − 1.57 to − 1.28), and Honduras (EAPC = -1.29, 95% UI − 1.42 to − 1.16). By 2017, the estimated global incidence of asthma had decreased considerably with age, especially in people younger than 10. However, the incidence of asthma recorded for people aged 65 – 74 slightly increased during this period.

Etiology and Causal Factors of Asthma

The most widely studied trigger factor for the presentation of asthma is atopy or the increased production of immunoglobulin E (IgE) antibodies as a biological response to allergen exposure. About fifty-six percent of all asthma cases were linked to different types of atopies in studies conducted by the National Health and Nutrition Examination Survey III (NHANES III). The value was extracted from data insights of about 12,106 asthma screenings between 1988 and 1994. Sustained exposure of allergic patients to inhaled allergens directly increases the risks of airway remodeling, airway hyperresponsiveness, and other classic asthma symptoms. However, the complexities of personal life and health as it spans nutrition, personal care, sex, and occupation make the risk of asthma variable.

Environmental Pollution

In epidemiological studies focused on examining possible links between asthma prevalence and industrialization, researchers found a substantial disparity among urban children compared to non‐urban children. These observations have been consistently reported for the last two decades. The wide distribution of pest allergens, poisonous atmospheric discharges, and mice and cockroaches in non-urban areas have been implicated in the disproportional prevalence of asthma in non-urban children. In addition, a considerable accumulation of research evidence suggests that the indoor concentration of pollutants is increasingly becoming higher than the outdoor concentration in the United States; this is also true for European urban communities. Secondhand exposure to indoor pollutants, including particulate matter (PM), asbestos, and nitrogen dioxide (NO2), has also been independently linked to the onset of asthma cases in children and young adults (Grant & Wood, 2022).

It has been shown that environmental interventions can reduce relevant indoor allergen and pollutant exposures, and they are associated with clear improvements in asthma. The best‐studied indoor pollutants linked to the high incidence of asthma in urban and non-urban areas include airborne PM and NO2. Airborne PM is measured based on the dimension of fractions, so fine has an aerodynamic diameter of 2.5 μm or less, and coarse PM has an aerodynamic diameter between 2.5 μm and 10 μm. Research has consistently highlighted the impact of these PMs on the development of asthma in the general population (Vardoulakis et al., 2020).


In addition to increasing the risks of the respiratory effects of air pollution, obesity has been proven to increase the risk of asthma based on prognosis and phenotype. Many epidemiological studies have repeatedly highlighted the common theme of asthma development and obesity across different population clusters globally. In these clusters, airway functioning is progressively impaired in obese individuals with a complication of asthma, generally resulting in symptom exacerbation, reduced life quality, impaired social functioning, and increased mortality index. Judging from available evidence, different immunological mechanisms and increased airway inflammation commonly described in both disorders have established a strong link between asthma and obesity. Although the mechanism of connection between asthma and obesity is still under investigation, recent research reports have demonstrated significant evidence suggesting an increased risk of asthma diagnosis in obese patients (Ying et al., 2022).

In addition to increasing the risk of developing asthma, immunological responses and decreased respiratory function may also converge to enhance airway inflammation and complicate asthma therapy in obese patients; this explains the altered response to glucocorticoid therapy observed in obese patients (Tooba & Wu, 2022). Typical symptoms of asthma also appear to be more severe in obese patients. Obese patients report more frequency and severity of dyspnea and asthma symptoms caused by mechanical impedance to airflow and inadequate lung function.

Occupational Risk Factors

The occupational environment is widely considered a significant risk factor in asthmatics, with the impact directly measurable on disease onset and severity of symptomatic exacerbations. Multiple epidemiological studies have reported that occupational asthma is often underreported and underdiagnosed. Asthma exacerbations relating to occupational risk factors can significantly impact disease progression and the overall mortality risk. Traditionally, the most commonly studied triggers in occupational asthma are classified into two broad classes; high–molecular weight compounds (HMW) and low–molecular weight compounds (LMW) (Jaakkola et al., 2021). The most relevant sensitizer belonging to the HMW class include flour dust, enzymes (plant and animal-derived), gums, foods, tobacco, rubber‐derived proteins, animal‐derived and insect‐derived allergens, and seafood–derived allergens. Those in the LMW class include Western red cedar, polyisocyanates and their polymers, acid anhydrides, metals, and a spectrum of chemical substances. In many cases, the outcome of asthma depends on these triggers, as patients sometimes disregard the effect of occupational risk factors. Properly evaluating these triggers and their effects significantly impacts the future of employment, health, and life quality (Wolf et al., 2020).

Clinical Evaluation and Symptomatology of Asthma

Today, the most widely recognized clinical evaluation procedure for the initial diagnosis and confirmation of asthma cases is outlined by the 2022 edition of the Global Strategy for Asthma Management and Prevention (GINA).

Diagnosing asthma in patients not currently placed on a controller regimen is based on recognizing the nature and expression of the basic symptoms of asthma, including wheezing, shortness of breath, chest tightness or cough, and significant limitation in expiratory airflow as determined by spirometry. Understanding the pattern of symptoms is clinically significant, as respiratory symptoms may be linked to other conditions with similar symptomatic presentations (Felix et al., 2021). If possible, the evidence supporting a diagnosis of asthma as observed by the clinician should be recorded at the first presentation to enable fact-based monitoring of symptom resolution or exacerbation. Monitoring the patient is also essential to determine the effectiveness of selected controller therapy plans recommended for the patient.

As prescribed by GINA, the observatory tests and patterns of respiratory symptoms that are typical of an early-onset asthma case include:

  • Respiratory symptoms of wheezing, shortness of breath, cough, and/or chest tightness.
    • Adult patients and other demographic classes reported one or more of these symptoms.
    • Symptoms are severe in the nighttime and during the early hours of the day.
    • The severity of symptoms in count and intensity varies over time.
    • The most reported factors that trigger symptomatic breakdown generally include exercise, allergen exposure, changes in weather, laughter, or other irritants, including exhaust fumes, smoke, and pungent smells.

Other features that decrease the probability that respiratory symptoms are related to asthma onset include:

  • Separate reports of cough with no other severe symptoms suggesting airway impairment
  • Abnormal daytime and nighttime sputum production
  • Dyspnea (difficulty in breathing) complicated by dizziness, light-headedness, or peripheral tingling
  • Chest pain
  • Dyspnea due to physical exertion complicated with difficult inspiration
  • Lung Function Testing
    • Lung function testing is performed to ascertain the limitation levels in normal expiratory airflow. Asthma is characterized by variable expiratory airflow limitation due to a gradual reduction in expiratory lung function over time and to the extent that lung impairment is primarily linked to breathing complications in healthy patients. Since the severity and airway responsiveness vary significantly in people with asthma, lung function may also vary significantly. Greater variability in lung function has been reported in patients with poorly controlled asthma and allergenic response cases. Lung function testing should be carried out by well-trained healthcare professionals using standard equipment with absolute calibrations and a routine for maintenance.

The equipment usually recommends an inline filter to reduce the risk of microbial cross-contamination. The GINA update uses FEV1 from spirometry as the testing standard compared to peak expiratory flow (PEF). If PEF is selected over FEV1, it is recommended that the same meter be used repeatedly in subsequent measurements; this is due to reported cases of differences in measurement between different meters. A reduced FEV1 may indicate other lung conditions, poor spirometric technique, or faulty equipment. However, a reduced ratio of FEV1/FVC, compared with the lower limit of normal, is suggestive of significant impairment in both expiratory and inspiratory airflow. Many spirometers are now designed to include researched values based on multi-ethnic age-specific observations. In the medical care of asthma, once a significant impairment in airflow has been confirmed, the severity of airflow limitation is generally measured by observing the variation in both PEF and FEV1 under the same measurement conditions.

As GINA intended, variability is described as measurable improvements or deterioration in the symptoms associated with clinical impairment of the airways. These variabilities may be recognized daily or from a reversibility test as the patients respond to medications or as symptoms spontaneously resolve. Reversibility, in this sense, is described as a significant improvement in FEV1 or PEF, measured immediately after administering a rapid-acting bronchodilator, such as 200–400 mcg of salbutamol. In the place of salbutamol, a sustained controller treatment such as ICS may also be administered, with the observation period extended over a few days or weeks. In patients with typical respiratory symptoms, clinicians are advised to watch out for excessive changes in lung function as it concerns both expiration and inhalation. (Reddel et al., 2021). Some observations to specifically consider include:

  • A noticeable improvement in lung function following the administration of a controller bronchodilator.
  • A reduced lung functioning associated with a provocation test or a period of physical exertion.
  • Inconsistent variation in lung function judging from measurements taken repeatedly on separate visits of ambulatory monitoring over two weeks.
  • Bronchial Provocation Tests.
    • Healthcare professionals can also document variable expiratory airflow limitation by conducting a bronchial provocation test to directly ascertain the level of airway responsiveness. Agents used in this provocation test may include physical exertion, histamine, inhalable mannitol, and induced hyperventilation. Although the bronchial provocation test is moderately sensitive to biological impairments characteristic of asthma, it has limited specificity in differentiating between asthma and other respiratory conditions with a similar symptomatic profile.

Comorbidities and other conditions that impair biological functioning may affect the results of bronchial provocation tests. Recent studies have shown that airway hyperresponsiveness to inhaled methacholine differs in patients diagnosed with allergic rhinitis, cystic fibrosis, bronchopulmonary dysplasia, and COPD. These observations infer that a negative test in a patient not taking ICS can help to exclude asthma, but a positive test. It may not necessarily indicate an ongoing airway dysfunction as described in asthma pathology. To make a definitive diagnosis, the pattern of symptoms, nature of exacerbations, and other relevant clinical features that directly impact lung function should also be considered (Bins et al., 2020).

Clinical Intervention in Asthma Care

Based on multiple peer-reviewed publications on asthma care, the long-term goals of asthma therapy from a clinical perspective focus on achieving improved symptomatic control and minimizing the risk of exacerbations and asthma-related mortality. The pharmacological management of asthma, as prescribed by the recent update of GINA, includes the following.

Controller Medications

Controller medications generally contain ICS as the active pharmaceutical component. These medications are generally indicated for airway inflammation, allergic exacerbations, difficulty in breathing, and other symptoms that directly impair normal lung functioning. In mild asthmatic exacerbations, these medications may be administered using low-dose ICS-formoterol as needed. If indicated, these medications may be taken before physical exertion, especially in patients with symptoms linked to increased levels of physical exertion. The administration dose depends on the severity of the presentation of the symptoms. It should be titrated to minimize the risk of side effects while delivering maximum drug action at the minimum drug quantity.

Reliever Medications

Reliever medications are indicated to relieve asthmatic symptoms, including nighttime exacerbations immediately. Generally, they are widely recommended as prophylaxis for exercise-induced bronchoconstriction in asthmatics whose symptom severity is linked to physical exertion. Reliever medications are classified broadly into two categories – as-needed SABA and as-needed low-dose ICS-formoterol. Recently, pharmacological investigations have suggested that overuse of SABA may increase the overall risk of asthma exacerbations in many patients.

Therefore, dose optimization and response tracking are strongly advised in patients on these medications. Reducing and, ideally, eliminating the need for a SABA reliever is an essential goal in asthma management and a measure of asthma treatment success (Sharma et al., 2022). Eventually, eliminating the need for continuous prescription of a SABA is considered another important therapy goal of asthma care.

Initial Asthma Treatment Chart for Adults and Adolescents
Presenting SymptomsInitial TreatmentAlternative Initial Treatment
Asthma symptoms with no specific symptomatic pattern. This includes less than two exacerbations in a month, with no reports of exacerbations in the last year.As-needed low-dose ICS-formoterol.Separate or combined administration of low-dose ICS and SABA.
A need for a reliever medication regimen at least twice a month for symptom control.As-needed low-dose ICS-formoterol.Low-dose ICS with as-needed SABA. It is recommended that clinicians consider the risk of low medication adherence.
Severe exacerbation on most days of the week or nighttime awakenings occurring at least once a week.Low-dose ICS-formoterol maintenance and a reliever therapy plan.Consider low-dose ICS -LABA and as-needed SABA. Alternatively, medium-dose ICS and an as-needed SABA may be considered. The adherence index should be tracked.
Severe uncontrolled asthma and acute exacerbations on patient presentation.Reliever therapy plan and medium-dose ICS-formoterol. A short oral corticosteroid course is also indicated for effective symptom control.As-needed SABA with high-dose or medium-dose SABA. Clinicians may also consider a short course of oral corticosteroids administered under medical supervision and side effect monitoring. Although adherence is reportedly poor, high-dose ICS with as-needed SABA is another option.
(Reddel et al., 2021)
Initial Asthma Treatment Chart for Children Aged 6 -11 Years
Presenting SymptomsPreferred Initial Treatment
Asthmatic symptoms with no definite pattern, Symptomatic exacerbations occurring less than twice a month with no significant risk factor identified.As-needed SABA is the first option. Alternatively, ICS and SABA taken concurrently or separately may be considered.
A need for a reliever medication plan at least twice a month.As-needed SABA with low-dose ICS. Alternatively, clinicians may consider daily leukotriene receptor antagonists or the concurrent combination of SABA and ICS separately. The adherence index is important for improving symptom control.
Severe asthma symptoms occur most days of the week, or nighttime awakening secondary to symptoms exacerbations at least once a week.Low-dose ICS-LABA combined with as-needed SABA. Medium dose ICS combined with as-needed SABA. Low-dose ICS formoterol instituted as a reliever of maintenance therapy. Alternatively, clinicians may consider daily leukotriene receptor antagonists with as-needed SABA.
Patient presentation with severe asthma symptoms, uncontrolled and complicated with acute exacerbations.Institute a controller medication plan with medium-dose ICS combined with as-needed SABA. Low-dose ICS formoterol as a maintenance or reliever therapy plan.
Clinicians may also consider short course OCS.
(Reddel et al., 2021)


The term pneumoconiosis describes a group of heterogenous occupational CRDs caused by a series of inflammatory responses in the lung triggered by the accumulation of fine particles in the airway spaces. These fine particles associated with diagnosing pneumoconiosis are primarily linked to inorganic origin. They specifically include dust from coal mines, asbestos particles, silica deposits, and particles from mixed silicate. Pathologically, pneumoconiosis is characterized by chronic pulmonary inflammation complicated by fibrosis and significantly decreased lung function. In many patients, fibrotic pneumoconiosis predominates. Fibrotic pneumoconiosis is caused mainly by continued exposure to fine particles from silica, beryllium deposits, and talc (Vanka et al., 2022).

Between 1980 and 2014, an estimated 57,033 pneumoconiosis-related deaths were recorded in the United States alone. There are 15,163 deaths associated with asbestosis, 21,592 deaths associated with coal workers' pneumoconiosis, 4,529 deaths associated with silicosis, and 15,723 deaths associated with other causes of the condition. In 2014, epidemiological studies indicated large differences in mortality rates, with rates ranging from 0.1 to 43.5 fatalities per 100 000 inhabitants. In 2014, the vast majority reported extremely low mortality rates, with 91.0% reporting mortality rates of less than one death per 100 000. Mississippi, Colorado, Utah, and Montana have reported relatively high mortality rates.

With increased awareness and improved primary healthcare policies focused on reducing mortalities due to choric respiratory conditions, the mortality rate of pneumoconiosis declined by 48.5% overall between 1980 and 2014 as death per 100,00 population reduced from 0.9 to 0.6. Globally, the prevalence of pneumoconiosis differs specifically among regions. In 2013, 23,152 new cases of pneumoconiosis were reported in China, accounting for roughly 87.72% of all reported occupational diseases in China. In a recent update examining the newly available evidence on pneumoconiosis, DeLight N & Sachs (2022) reported an 8.1% increase in pneumoconiosis cases reported between 1990 to 2017, with the age-standardized prevalence rate significantly higher in males. According to the Global Burden of Disease Study, asbestosis makes up for the larger portion of pneumoconiosis-related deaths in developed countries, including the United Kingdom.

Etiology and Causal Factors of Pneumoconiosis

Pneumoconiosis is initiated by an inflammatory response to inhaled foreign particles. Inhaled dust stimulates the production of lymphocytes, macrophages, lymphocytes, and epithelial cells. Interleukin-1 beta, TNF-alpha, matrix metalloproteinases, and transforming growth factor-beta are then released by these cells. The dust-forming nodules are subsequently surrounded by fibroblasts stimulated to proliferate and expand. These nodules then result in extensive fibrosis, as seen in the lungs of coal workers, and silicosis (Kasuya et al., 2021). Occupation is the most significant risk factor in the pathophysiology of pneumoconiosis.

Pneumoconiosis TriggersOccupations with Increased Exposure Risk
Fibers from asbestos deposits, inflation materials, fireproofing, and manufacturing materials.Plumbers, roofers, mechanics, and shipyard workers.
Crystalline silica and fine particles from sand.Mine workers, sandblasters, stonemasons, and foundry agents.
Fine particles from mining activities and dust from coal.Mineworkers.
(DeLight & Sachs, 2022)

Clinical Evaluation and Symptomatology of Pneumoconiosis

The screening of pneumoconiosis primarily relies on observing a history of exposure to harmful dust and performing chest radiography.

To appropriately test for pneumoconiosis, chest tomography must be used to examine the progression of symptoms since exposure to hazardous triggers. The International Labor Organization (ILO) created the current standards describing the evaluation process. The most recent iteration of this evaluation was compiled in 2011 by the ILO International Classification of Radiographs of Pneumoconiosis (ILO/ICRP). Under this review guideline, the standards for medical imaging and the quality of diagnostic monitors required for pneumoconiosis screening were explicitly outlined (Qi et al., 2021). Currently, the National Institute for Occupational Safety and Health (NIOSH) of the United States certifies the competence of technicians tasked with reading and interpreting digital radiographs of suspected pneumoconiosis cases.

Even though high-resolution computed tomography (HRCT) is more sensitive than chest X-rays for the early detection of pneumoconiosis, the International Classification of HRCT for Occupational and Environmental Respiratory Diseases (ICOERD) has mandated the use of alternative diagnostic methods, particularly for occupational and environmental lung diseases (Qi et al., 2021). Since imaging techniques cannot independently assess the patient's functional status, pulmonary function tests (PFT) are commonly employed as a confirmatory standard for evaluating pneumoconiosis in patients exposed to trigger particles for an extended period. PFT can accurately evaluate the severity of dyspnea and differentiate between obstructive and restrictive illnesses (Li et al., 2022). Depending on the nature and severity of the disease, it may be challenging to identify pneumoconiosis from other airway disorders characterized by airway inflammation and decreased lung function. Today, medical professionals additionally require laboratory tests, such as bronchoalveolar lavage fluid (BALF), to determine the level of fine particle distribution in alveoli and large spaces.

Flow chart for the diagnosis of pneumoconiosis

Fig. 3. Flow chart for the diagnosis of pneumoconiosis adapted from Qi et al., 2021

Other clinical options currently under investigation as potential diagnostics standards for pneumoconiosis include electrical impedance tomography (EIT), three-dimensional magnetopneumography magnetic dipole model (3D-MPG-MDM), and the popular clinical diagnostic biomarker, microRNA (miRNA). Researchers have suggested that the nature of the biological conductance of electricity changes before the first set of clinical symptoms in early-onset pneumoconiosis. As an experimental diagnostic method, EIT has shown significant efficiency in accurately detecting changes in electrical conductivity to diagnose pneumoconiosis before the appearance of clinical symptoms (Yao et al., 2022). On the other hand, 3D-MPG-MDM can diagnose pneumoconiosis caused primarily by the accumulation of fine metal particles in the airways. 3D-MPG-MDM directly estimates disease risk and identifies the quantity of fine particles deposited in the lungs, thereby increasing the possibility of early diagnosis and improved disease prognosis.

Clinical Intervention in Pneumoconiosis

Although there is no cure for pneumoconiosis yet, the goal of treatment is to limit further lung damage. However, despite the significant increase in research interest in pneumoconiosis, established clinical interventions are still very limited. Today, the most widely referenced therapy involves varied regimens of inhalers, pulmonary rehabilitation, and oxygen. As it stands, these are used mainly in whole lung lavage and integrated treatment procedures. Integrated therapy plans for pneumoconiosis are based on the clinical conditions of the patient and the presentation of symptoms. Similarly, symptomatic therapy, management of comorbidities, and rehabilitative exercise regimens have significantly improved lung function and quality of life.

Clinical Management of Pneumoconiosis
Etiological TreatmentsWhole lung lavage: Inhibit inflammation and fibrosis
Symptomatic TreatmentsHealth management: Improve nutrition, increase physical strength, reduce dust
Integrated treatments: Anti-infection, oxygen therapy, treatment of complications
Surgical InterventionsLung transplant
(Qi et al., 2021)

Whole lung lavage removes phlegm, bronchial secretions, fine particles, and fibrotic cytokines from the airway for patients managed for pneumoconiosis. Lavage can be considered in the early and late stages of the disease. However, it works best when instituted in the early-stage therapy plan, when the largest deposits of fine particles are still limited to the pulmonary alveoli. However, the evidence supporting whole lung lavage as a beneficial procedure in reversing lung function in pneumoconiosis is weak and highly controversial. As an invasive procedure, there is evidence that whole lung lavage may have a long-term effect on the normal process of lung homeostasis.

Performing lung transplantation is a feasible method for end-stage lung diseases, including silicosis, and is most promising in young patients. In addition, some drugs have recently been identified as potential therapeutic options for pneumoconiosis (Hoy et al., 2022).

The drugs include:

  • Pirfenidone is an anti-fibrotic drug indicated for idiopathic pulmonary fibrosis (IPF) (Miedema et al., 2022).
  • The anti-inflammatory immune response drugs, hydroxychloroquine, infliximab, and corticosteroids (Kaida et al., 2022).
  • The antioxidant drug N-acetylcysteine (Tian et al., 2020).
  • Vasodilators nicorandil and carvedilol (Xu et al., 2022).

The vasodilators significantly reduce the risk of pulmonary inflammation in animal models with pneumoconiosis. Corticosteroids with anti-inflammation properties have also shown noticeable effects in reducing the severity of symptoms presented in pneumoconiosis. In animal models, many traditional Chinese medicine extracts have shown significant clinical properties in relieving the fibrosis and inflammation related to asbestosis and silicosis. The extracts include dioscin, astragaloside IV, kaempferol, tanshinone IIA, and dihydrotanshinone.

Role of Nursing Care Teams in the Management of Chronic Respiratory Diseases

The role of nursing care services in CRDs dates back to the early 80s, with the establishment of specialist nurses in the United States specializing in respiratory care. Care plans during this era were designed to include homes-based, in-patient, and ambulatory respiratory care for CRD patients. Today, these specialized care services are nonexistent in many countries due to insufficient evidence to demonstrate their cost-effectiveness. In countries with a vast infrastructure to support this specialized care, nurses explore different problem-based learning and standard medical management plans to impact the prognosis of CRDs positively. In a wide context, some of the basic nursing interventions for CRD patients include information collection, knowledge acquisition, and attitude generation.

  • Information collection
    • Nursing teams collate, record, and update information that directly measures the psychological and health well-being of the patients. The preliminary record collection guides the care team on therapy plan design and execution.
  • Acquisition of knowledge
    • In this phase, specialist nurses may provide information related to the healthcare status of the patients, thereby playing significant intermediary roles in helping patients understand the basis for the different care plans instituted. Responses can also be documented in this stage. Nursing intervention in this stage may also include helping patients modify their lifestyle and adopting beneficial respiratory exercise routines.
  • Attitude generation
    • At this stage, the nurses' objective is to urge all patients to maintain a good outlook. The nursing staff keeps learning and reviewing the material covered in the pre-discharge health course. Nurses must constantly evaluate patients’ daily behavior and knowledge, collect data on the patient's behavior change, and identify the primary factors impeding the patient's behavior change.
    • In this phase, a nursing specialist may reassure the patient by discussing the clinical improvements made with medication use. Discussion might also include pre-discharge health, social living, and mental well-being education. The daily behaviors and clinical responses of patients can also be documented during this phase; this helps the medical team understand factors that may contribute to behavior modification in these patients.
  • Practice Formation
    • In this final phase, nurses encourage patients to consistently maintain a positive outlook and other good habits learned during therapy. Nursing intervention during this stage should revolve around proper health education, maintaining healthy habits, and conducting personalized interventions as appropriate for each patient.

Case Study

Jackson Neville worked for ten years at a diamond mine in South Africa. Rising through the ranks as an unskilled mine worker, Jackson moved quickly from being a deep-earth mining artisan to an artisan supervisor. However, for the ten years of active service, Jackson's daily work routine unavoidably involves spending hours inhaling small particulate matters of mining by-products.

Now a 72-year-old retired mining artisan, Jackson's respiratory health has consistently failed. He found it difficult to hold deep breaths and continuously complained of flank pain. His cheap insurance coverage got him ibuprofen; however, this did not help. The pain increased to include painful abdominal sensations accompanied by forced breathing.

History of Present Illness

Jackson experienced a sudden respiratory failure and presented to the emergency ward with complaints of breathlessness. His long-standing hypertension and coronary artery disease have been poorly controlled on medications for a long time. He also had a history of two separate events of myocardial infarctions. About one week before the presentation, he had chest pain lasting about 30 minutes.

Since the first presentation, his breathlessness has significantly worsened to where he cannot comfortably walk across a room or perform physical tasks that require minimal exertion. He also has severe shortness of breath when lying down. Occasionally, his breathing condition improved when propped with support such as pillows.

Clinical Examination

On examination, he is afebrile, with a blood pressure of 156/121 mm Hg, heart rate of 110/min, respiratory rate of 33/min, and oxygen saturation of 79% on room air. He appears pale, and his jugular venous pressure measures 11 cm H2O.

His Lung CT showed multiple small, calcified nodules that are subpleural and perilymphatic with sharp margins, found mainly in the upper lobe. In some regions, nodules coalesce into progressive massive fibrosis with well-defined punctate calcifications in hilar and mediastinal lymph nodes.

On cardiac examination, he was classed tachycardiac, with an audible S3 and S4. Murmurs and rubs were not detected, and the extremities showed no sign of progressive edema. ECG examination reported left ventricular hypertrophy and Q waves in the anterior and lateral leads, consistent with his history of hypertension and myocardial infarction. Chest radiography showed progressive massive opacities with irregular borders consistent with a diagnosis of pneumoconiosis. If diagnosed at an advanced stage, silicosis shows subsequent nodule convergence, with multiple convergences forming lesions with multiple foci. A central region with collagen and macrophage may be present.


He was admitted to the ICU with a diagnosis of silicosis and possibly myocardial infarction. He was started on Ceftriaxone for antibiotic coverage, pirfenidone, and hydroxychloroquine. Pirfenidone inhibits epithelial-mesenchymal transition, while hydroxychloroquine blocks toxicity and lysosomal membrane permeability. Jackson was also started on a pulmonary rehabilitation regimen complemented with oxygen therapy. Jackson's case is one of the thousands of pneumoconiosis cases reported yearly by miners in different parts of the world. Over three months of therapy, Jackson's breathing difficulties have significantly improved. However, his radiography examinations still show prominent parenchymal damage as silicotic nodules remain consistent in outlay.


CRDs contribute to the ongoing global health burden. COPD, asthma, and pneumoconiosis are the most common respiratory conditions affecting people worldwide. Each condition can cause morbidity and mortality. An accurate assessment of symptomatology should occur to rule out similar conditions. Treatment is aimed at reducing symptoms and the mortality of these diseases.

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Implicit Bias Statement

CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.


  • Agarwal, A. K., Raja, A., & Brown, B. D. (2022). Chronic Obstructive Pulmonary Disease. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
  • American Thoracic Society (ATS). (2019). Chronic Obstructive Pulmonary Disease (COPD). American Thoracic Society (ATS). Visit Source.
  • Bai, J., Zhao, Y., Yang, D., Ma, Y., & Yu, C. (2022). Secular trends in chronic respiratory diseases mortality in Brazil, Russia, China, and South Africa: a comparative study across main BRICS countries from 1990 to 2019. BMC public health, 22(1), 91. Visit Source.
  • Bins, J. E., Metting, E. I., Muilwijk-Kroes, J. B., Kocks, J. W. H., & In 't Veen, J. C. C. M. (2020). The use of a direct bronchial challenge test in primary care to diagnose asthma. NPJ primary care respiratory medicine, 30(1), 45. Visit Source.
  • Bitan, M., Steinberg, D. M., Wilson, S. R., Kalkbrenner, A. E., Lanphear, B., Hovell, M. F., Gamliel, V. M., & Rosen, L. J. (2022). Association between objective measures and parent-reported measures of child tobacco smoke exposure: A secondary data analysis of four trials. Tobacco induced diseases, 20, 62. Visit Source.
  • Chang, J. T., Meza, R., Levy, D. T., Arenberg, D., & Jeon, J. (2021). Prediction of COPD risk accounting for time-varying smoking exposures. PloS one, 16(3), e0248535. Visit Source.
  • Clini, E., & Costi, S. (2021). Looking Ahead in Pulmonary Rehabilitation. Frontiers in rehabilitation sciences, 1, 615545. Visit Source.
  • Crapo, J., Gupta, A., Lynch, D. A., Vogel-Claussen, J., Watz, H., Turner, A. M., Mroz, R. M., Janssens, W., Ludwig-Sengpiel, A., Beck, M., Langellier, B., Ittrich, C., Risse, F., & Diefenbach, C. (2021). FOOTPRINTS study protocol: rationale and methodology of a 3-year longitudinal observational study to phenotype patients with COPD. BMJ open, 11(3), e042526. Visit Source.
  • Czira, A., Banks, V., Requena, G., Wood, R., Tritton, T., Wild, R., Compton, C., Duarte, M., & Ismaila, A. S. (2022). Characterisation of patients with chronic obstructive pulmonary disease initiating single-device inhaled corticosteroids/long-acting β2-agonist dual therapy in a primary care setting in England. BMJ open respiratory research, 9(1), e001243. Visit Source.
  • Dekkers, B. G. J., Saad, S. I., van Spelde, L. J., & Burgess, J. K. (2021). Basement membranes in obstructive pulmonary diseases. Matrix biology plus, 12, 100092. Visit Source.
  • DeLight, N, & Sachs, H. Pneumoconiosis. (2022). In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
  • Eenjes, E., Tibboel, D., Wijnen, R. M. H., & Rottier, R. J. (2022). Lung epithelium development and airway regeneration. Frontiers in cell and developmental biology, 10, 1022457. Visit Source.
  • European Respiratory Society (ERS). (n.d.). Living well with COPD. European Respiratory Society (ERS). Visit Source.
  • Felix, S. N., Agondi, R. C., Aun, M. V., Olivo, C. R., de Almeida, F. M., Amorim, T. S., Cezario, J. C., Giavina-Bianchi, P., Tiberio, I. F. L. C., de Martins, M. A., & Romanholo, B. M. S. (2021). Clinical, functional and inflammatory evaluation in asthmatic patients after a simple short-term educational program: a randomized trial. Scientific reports, 11(1), 18267. Visit Source.
  • GBD 2015 Chronic Respiratory Disease Collaborators (2017). Global, regional, and national deaths, prevalence, disability-adjusted life years, and years lived with disability for chronic obstructive pulmonary disease and asthma, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. The Lancet. Respiratory medicine, 5(9), 691–706. Visit Source.
  • GBD Chronic Respiratory Disease Collaborators (2020). Prevalence and attributable health burden of chronic respiratory diseases, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet. Respiratory medicine, 8(6), 585–596. Visit Source.
  • Grant, T. L., & Wood, R. A. (2022). The influence of urban exposures and residence on childhood asthma. Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, 33(5), e13784. Visit Source.
  • Hoy, R. F., Jeebhay, M. F., Cavalin, C., Chen, W., Cohen, R. A., Fireman, E., Go, L. H. T., León-Jiménez, A., Menéndez-Navarro, A., Ribeiro, M., & Rosental, P. A. (2022). Current global perspectives on silicosis-Convergence of old and newly emergent hazards. Respirology (Carlton, Vic.), 27(6), 387–398. Visit Source.
  • Jaakkola, M. S., Lajunen, T. K., Heibati, B., Wang, Y. C., Lai, C. H., & Jaakkola, J. J. K. (2021). Occupation and subcategories of asthma: a population-based incident case-control study. Occupational and environmental medicine, 78(9), 661–668. Visit Source.
  • Kaida, H., Utsunomiya, T., Koide, Y., Ueda, Y., Wada, K., Yoshida, Y., Kinoshita, Y., Kushima, H., & Ishii, H. (2022). A case of welder's pneumoconiosis treated with corticosteroid followed by nintedanib. Respiratory medicine case reports, 39, 101729. Visit Source.
  • Kasuya, Y., Kim, J. D., Hatano, M., Tatsumi, K., & Matsuda, S. (2021). Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis. International journal of molecular sciences, 22(11), 6041. Visit Source.
  • Li, T., Yang, X., Xu, H., & Liu, H. (2022). Early Identification, Accurate Diagnosis, and Treatment of Silicosis. Canadian respiratory journal, 2022, 3769134. Visit Source.
  • Miedema, J. R., Moor, C. C., Veltkamp, M., Baart, S., Lie, N. S. L., Grutters, J. C., Wijsenbeek, M. S., & Mostard, R. L. M. (2022). Safety and tolerability of pirfenidone in asbestosis: a prospective multicenter study. Respiratory research, 23(1), 139. Visit Source.
  • Mikolasch, T. A., Oballa, E., Vahdati-Bolouri, M., Jarvis, E., Cui, Y., Cahn, A., Terry, R. L., Sahota, J., Thakrar, R., Marshall, P., & Porter, J. C. (2022). Mass spectrometry detection of inhaled drug in distal fibrotic lung. Respiratory research, 23(1), 118. Visit Source.
  • Proboszcz, M., Goryca, K., Nejman-Gryz, P., Przybyłowski, T., Górska, K., Krenke, R., & Paplińska-Goryca, M. (2021). Phenotypic Variations of Mild-to-Moderate Obstructive Pulmonary Diseases According to Airway Inflammation and Clinical Features. Journal of inflammation research, 14, 2793–2806. Visit Source.
  • Qi, X. M., Luo, Y., Song, M. Y., Liu, Y., Shu, T., Liu, Y., Pang, J. L., Wang, J., & Wang, C. (2021). Pneumoconiosis: current status and future prospects. Chinese medical journal, 134(8), 898–907. Visit Source.
  • Reddel, H. K., Bacharier, L. B., Bateman, E. D., Brightling, C. E., Brusselle, G. G., Buhl, R., Cruz, A. A., Duijts, L., Drazen, J. M., FitzGerald, J. M., Fleming, L. J., Inoue, H., Ko, F. W., Krishnan, J. A., Levy, M. L., Lin, J., Mortimer, K., Pitrez, P. M., Sheikh, A., Yorgancioglu, A. A., … Boulet, L. P. (2021). Global Initiative for Asthma Strategy 2021: executive summary and rationale for key changes. The European respiratory journal, 59(1), 2102730. Visit Source.
  • Rocha, V., Severo, M., Ramos, E., Falcão, H., Stringhini, S., & Fraga, S. (2021). Socioeconomic circumstances and lung function growth from early adolescence to early adulthood. Pediatric research, 90(6), 1235–1242. Visit Source.
  • Sharma, S., Hashmi, M. F., & Chakraborty, R. K. (2022). Asthma Medications. In StatPearls. StatPearls Publishing.
  • Shuai, T., Zhang, C., Zhang, M., Wang, Y., Xiong, H., Huang, Q., & Liu, J. (2021). Low-dose theophylline in addition to ICS therapy in COPD patients: A systematic review and meta-analysis. PloS one, 16(5), e0251348. Visit Source.
  • Singh, D., Agusti, A., Anzueto, A., Barnes, P. J., Bourbeau, J., Celli, B. R., Criner, G. J., Frith, P., Halpin, D. M. G., Han, M., López Varela, M. V., Martinez, F., Montes de Oca, M., Papi, A., Pavord, I. D., Roche, N., Sin, D. D., Stockley, R., Vestbo, J., Wedzicha, J. A., … Vogelmeier, C. (2019). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. The European respiratory journal, 53(5), 1900164. Visit Source.
  • Thomen, R. P., Woods, J. C., Sturm, P. F., Jain, V., Walkup, L. L., Higano, N. S., Quirk, J. D., & Varisco, B. M. (2020). Lung microstructure in adolescent idiopathic scoliosis before and after posterior spinal fusion. PloS one, 15(10), e0240265. Visit Source.
  • Tian, H., Zhou, Y., Tang, L., Wu, F., Deng, Z., Lin, B., Huang, P., Wei, S., Zhao, D., Zheng, J., Zhong, N., & Ran, P. (2020). High-dose N-acetylcysteine for long-term, regular treatment of early-stage chronic obstructive pulmonary disease (GOLD I-II): study protocol for a multicenter, double-blinded, parallel-group, randomized controlled trial in China. Trials, 21(1), 780. Visit Source.
  • Tooba, R., & Wu, T. D. (2022). Obesity and asthma: A focused review. Respiratory medicine, 204, 107012. Visit Source.
  • Tsiligianni, I., & Kocks, J. W. H. (2020). Daytime symptoms of chronic obstructive pulmonary disease: a systematic review. NPJ primary care respiratory medicine, 30(1), 6. Visit Source.
  • Vanka, K. S., Shukla, S., Gomez, H. M., James, C., Palanisami, T., Williams, K., Chambers, D. C., Britton, W. J., Ilic, D., Hansbro, P. M., & Horvat, J. C. (2022). Understanding the pathogenesis of occupational coal and silica dust-associated lung disease. European respiratory review : an official journal of the European Respiratory Society, 31(165), 210250. Visit Source.
  • Vardoulakis, S., Giagloglou, E., Steinle, S., Davis, A., Sleeuwenhoek, A., Galea, K. S., Dixon, K., & Crawford, J. O. (2020). Indoor Exposure to Selected Air Pollutants in the Home Environment: A Systematic Review. International journal of environmental research and public health, 17(23), 8972. Visit Source.
  • Wang, C., Zhou, J., Wang, J., Li, S., Fukunaga, A., Yodoi, J., & Tian, H. (2020). Progress in the mechanism and targeted drug therapy for COPD. Signal transduction and targeted therapy, 5(1), 248. Visit Source.
  • Wolf, M., & Lai, P. S. (2020). Indoor Microbial Exposures and Chronic Lung Disease: From Microbial Toxins to the Microbiome. Clinics in chest medicine, 41(4), 777–796. Visit Source.
  • Xie, M., Liu, X., Cao, X., Guo, M., & Li, X. (2020). Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017. Respiratory research, 21(1), 49. Visit Source.
  • Xu, J., Zhao, S., Zhao, L., & Sun, M. (2022). Carvedilol alleviates lipopolysaccharide (LPS)-induced acute lung injury by inhibiting Ras homolog family member A (RhoA)/ROCK activities. Bioengineered, 13(2), 4137–4145. Visit Source.
  • Yao, Y., Wei, T., Zhang, H., Xie, Y., Gu, P., Yao, Y., Xiong, X., Peng, Z., Zhen, Z., Liu, S., Cui, X., Mei, L., & Ma, J. (2022). Characteristics of Diagnosed and Death Cases of Pneumoconiosis in Hubei Province, China, 1949-2019. International journal of environmental research and public health, 19(23), 15799. Visit Source.
  • Ying, X., Lin, J., Yuan, S., Pan, C., Dong, W., Zhang, J., Zhang, L., Lin, J., Yin, Y., & Wu, J. (2022). Comparison of Pulmonary Function and Inflammation in Children/Adolescents with New-Onset Asthma with Different Adiposity Statuses. Nutrients, 14(14), 2968. Visit Source.
  • Zeng, L. H., Hussain, M., Syed, S. K., Saadullah, M., Jamil, Q., Alqahtani, A. M., Alqahtani, T., Akram, N., Khan, I. A., Parveen, S., Fayyaz, T., Fatima, M., Shaukat, S., Shabbir, N., Fatima, M., Kanwal, A., Barkat, M. Q., & Wu, X. (2022). Revamping of Chronic Respiratory Diseases in Low- and Middle-Income Countries. Frontiers in public health, 9, 757089. Visit Source.
  • Zhang, D. D., Liu, J. N., Ye, Q., Chen, Z., Wu, L., Peng, X. Q., Lu, G., Zhou, J. Y., Tao, R., Ding, Z., Xu, F., & Zhou, L. (2021). Association between socioeconomic status and chronic obstructive pulmonary disease in Jiangsu province, China: a population-based study. Chinese medical journal, 134(13), 1552–1560. Visit Source.