Introduction
Huether and McCance (2016) define asthma as an “inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constriction of the airways, and variable airflow obstruction that is reversible” (p. 698).
The major distinction of chronic asthma (CA) from acute asthma exacerbation (AAE) is that an acute condition implies a rapid onset of adverse symptoms and a relatively short-term duration, while the term “chronic” refers to an enduring aggravated condition progressing in a slow manner. The two conditions have both similar and distinct features which will be discussed in the following paragraphs along with their pathophysiological mechanisms, diagnosis, and available treatment procedures.
CA: Pathophysiology
In a simplified form, the pathogenesis of bronchial asthma can be represented as a combination of two basic mechanisms: chronic inflammation of the respiratory tract and bronchial hyperresponsiveness. The inflammatory process in the bronchi leads to the obstruction of the airways causing a decrease in the airflow. These functional changes cause such symptoms of bronchial asthma as dyspnea, cough, chest tightness, and wheezing.
The narrowing of the bronchial lumen in CA is the result of the action of numerous factors. The main one is the contraction of the smooth muscles of the bronchi, caused by the action of agonists, such as histamine, released from the inflammatory cells (Janssen, 2012).
The consequences of the smooth muscles’ tightening can be aggravated by the thickening of the bronchial wall due to acute edema, cellular infiltration, and remodeling of the airways − chronic hyperplasia of smooth muscles, vessels, and secretory cells, and the deposition of the matrix in the bronchus wall (Janssen, 2012). Obstruction is exacerbated by a tight, viscous discharge produced by goblet cells (Janssen, 2012).
Hyperreactivity of the bronchi is a state when they narrow either too easily or too much in response to various provoking factors. As noted by Bjørke-Monsen et al. (2017), this process is “mediated via airway smooth muscle tone and is modulated by the autonomic nervous system, nitric oxide, and airway inflammation” (p. 83). Moreover, in patients with CA, excess sputum in the airways is accumulated over time, and it strengthens the response of the bronchi to external stimuli leading to spasms and, in this way, also affecting the volume and the composition of sputum. The substances released in the inflammatory cascade including epidermal growth factors, IL-4, IL-9, and IL-13, etc. play the primary role in this process (Ha & Rogers, 2015).
AAE: Pathophysiology
AAE differs from the chronic condition mainly by its association with a rapid onset of severe bronchial obstruction. AAE-related bronchospasm results in the increase of the residual capacity of the lungs, a decreased volume of reserve breath and exhalation, acute shortness of breath, and impaired venous return of blood to the heart, etc. (Niimi, Lewis, & Fanning, 2015) These alterations promote the development of pulmonary hypertension. Reduction of venous return of blood contributes to fluid retention in the body due to the increase in the level of antidiuretic hormone and aldosterone (Gershwin & Halpern, 2012).
Moreover, the condition leads to hypoxia − the deprivation of the organism from oxygen. The dysfunction of external respiration and cardiovascular system disrupts the acid-base balance and gas composition of the blood (Gershwin & Halpern, 2012). As a result, some organs can undergo a process of irreversible transformations.
Contributing Factors: Gender and Ethnicity
Gender and ethnicity indirectly affect asthma incidence. Researchers observe that the prevalence of CA in a particular demographic group is rather determined by gender- or ethnicity-specific socioeconomic and environmental factors. For instance, Greenblatt, Mansour, Zhao, Ross, and Himes (2017) observe that the rate of asthma development in Native Americans and Alaskan Natives is higher than in Whites because these minority populations are associated with low economic status and exposure to adverse environmental influences.
The researchers note as well that “individuals of both genders living below the poverty line” are “at increased risk of having asthma” (Greenblatt et al., 2017, p. 2). Such multicultural behavioral indicators as engagement in physical activity, overeating and unhealthy dieting leading to overweight and obesity, smoking, etc. also proved to increase the risk for asthma occurrence in the study by Zahran and Bailey (2013).
To identify which behavioral factors contribute to asthma development in an individual of any gender or ethnic background, the health practitioner should carry out a holistic assessment of all systems relevant to the patient’s health including the psycho-social, ecological, and cultural ones. Additionally, to differentiate asthma from other similar respiratory disorders, Brigham and West (2015) suggest using spirometry − a tool that allows the detection of any functional abnormalities in the lungs. At the same time, AAE can be diagnosed through the assessment of blood gas composition because the level of carbon dioxide in plasma in this condition is significantly elevated.
When speaking of treatment methods, lifestyle interventions addressing reduce ethnicity- and gender-specific behavioral peculiarities may help reduce asthma symptoms. Based on the results of the patient assessment, the practitioner can recommend him/her to make some changes in nutrition, physical activity, environment, and so on. Along with this, pharmacologic remedies can be prescribed for distinct asthmatic events and situations.
For example, beta-agonists can be used to relieve CA symptoms, while glucocorticosteroids will help against inflammation (Institute for Clinical Systems Improvement, 2012). When speaking of AAE treatment, researchers recommend to implement the following steps: treat hypoxemia, provide the patient with ß2-agonists and corticosteroids, evaluate the response to treatment, and make alterations if needed (Ortiz-Alvarez, Mikrogianakis, & Canadian Paediatric Society, Acute Care Committee, 2012).
β-2-agonists can be regarded as the first-line drugs in the treatment of bronchospasm attacks because they help relieve adverse symptoms in a short time. However, they can induce arrhythmia, arterial hypertension, agitation, and so on. Thus, these drugs should be used with greater care in patients with cardiovascular conditions.
References
Bjørke-Monsen, A., Vollsæter, M., Ueland, P. M., Markestad, T., Øymar, K., & Halvorsen, T. (2017). Increased bronchial hyperresponsiveness and higher asymmetric dimethylarginine levels after fetal growth restriction. American Journal of Respiratory Cell and Molecular Biology, 56(1), 83-89. Web.
Brigham, E. P., & West, N. E. (2015). Diagnosis of asthma: Diagnostic testing. International Forum of Allergy & Rhinology, 5(S1). Web.
Gershwin, M. E., & Halpern, G. M. (2012). Bronchial asthma: Principles of diagnosis and treatment. New York, NY: Springer.
Greenblatt, R., Mansour, O., Zhao, E., Ross, M., & Himes, B. E. (2017). Gender-specific determinants of asthma among U.S. adults. Asthma Research and Practice, 3, 2. Web.
Ha, E. V., & Rogers, D. F. (2015). Novel therapies to inhibit mucus synthesis and secretion in airway hypersecretory diseases. Pharmacology, 97(1-2), 84-100. Web.
Huether, S. E., & McCance, K. L. (2016). Understanding pathophysiology. St. Louis, MO: Mosby/Elsevier.
Janssen, L. J. (2012). Airway smooth muscle as a target in asthma and the beneficial effects of bronchial thermoplasty. Journal of Allergy, 2012, 593784. Web.
Niimi, K. S., Lewis, L. S., & Fanning, J. J. (2015). Impairment of venous drainage on extracorporeal membrane oxygenation secondary to air trapping in acute asphyxial asthma. The Journal of Extra-Corporeal Technology, 47(2), 109–112.
Ortiz-Alvarez, O., Mikrogianakis, A., & Canadian Paediatric Society, Acute Care Committee. (2012). Managing the paediatric patient with an acute asthma exacerbation. Paediatrics & Child Health, 17(5), 251–256.
Zahran, H. S., & Bailey, C. (2013). factors associated with asthma prevalence among racial and ethnic groups—United States, 2009–2010 behavioral risk factor surveillance system. Journal of Asthma, 50(6), 583-589. Web.