Asthma is a pulmonary condition that may be characterized by either a chronic or acute inflammation of the respiratory tubes compounded with constriction of the respiratory tract smooth muscles. According to Pola-Bibian et al. (2016), an asthma exacerbation is the worsening of the symptoms and lung function, sometimes during or following the completion of asthma therapy and may require further medication or hospitalization. Effective determination of asthma’s exacerbation, diagnosis, and proper treatment, and management depends on identifying the correct pathophysiological mechanism of the condition. Sears (2015) points out that cigarette smoking is the most prevalent trigger mechanism for adult-onset respiratory conditions associated with obstructive pulmonary disease. This paper discusses the pathophysiological process in acute and chronic asthma due to cigarette smoking, as well as the diagnosis and treatment for a patient diagnosed with smoking-induced asthma.
The pathophysiological exacerbation of chronic asthma due to cigarette smoking is as a result of alteration of the airways inflammatory cell phenotypes. This includes reduced eosinophil or increased neutrophils. Also, changes in the expression of the α to β ratio of glucocorticoids and elevated activation of inflammatory mediator transcription factors are involved in chronic asthma due to cigarette smoking (Wart & Gibson, 2005). According to Kumar, Herbert & Foster (2015), chronic asthma attacks occur over a long period during which the arterial blood patterns are not sporadically affected. Partial blood oxygen concentrations will slightly fall from 100 mm Hg to approximately 85 mm Hg coupled with a slight pH increase from 7.45 to 7.40. The changes in the arterial blood patterns and pH are necessary for the clearance of the viral infection. These changes, however, occur concomitantly with the inflammation process thereby stirring symptomatology that accelerates the decline of lung function and compliance. The overall outcome is worsening the severity of the condition and reducing the responsiveness to glucocorticoids ( Graham & Eid, 2015).
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The mechanism involved in chronic asthma due to cigarette smoking is increased bronchial hyper-responsiveness which leads to bronchospasms and airway obstruction (Sears, 2015). Bronchospasm is associated with shortness of breath and typical symptoms of wheezing and coughing. Chronic airway inflammation is due to an imbalance between the Th lymphocyte populations – Th1 and Th2. Th lymphocytes are responsible for the production of cytokines which play a role in inflammatory processes. Cytokine imbalance triggered by cigarette smoking causes persistent inflammation of the airway (Kumar, Herbert, & Foster, 2016). Resistance to airflow due to airway obstruction and inflammation in exacerbated conditions reduces the expiratory flow rates and may result in hyperinflation to compensate for the airflow obstruction. However, alveolar hypoventilation occurs when the tidal volume is closer to the pulmonary dead space, during which the compensation mechanism is limited. Increased hyperinflation, alveolar hypoventilation and the uneven distribution of air cause ventilation-perfusion mismatch. Prolonged ventilation-perfusion mismatch causes increased CO 2 retention (a high PaCO 2 ).
The pathophysiological mechanism of exacerbation in acute asthma due to cigarette smoking involves an immunologic response on exposure to the cigarette smoke. Smoking triggers an inflammatory burden for the lower respiratory tract in a number of related but different pathophysiological mechanisms. According to Wark & Gibsob (2006), these mechanisms include alteration of the inflammatory and epithelial cell subtypes, increased recruitment of the inflammatory cells, and augmentation of cellular function through an enhanced release of pro-inflammatory mediators. The airway inflammation can also be amplified through the release of increased levels of cysteinyl leukotrienes. Acute bronchoconstriction triggered by the release of IgE dependent inflammatory mediator and is the primary component of the acute asthmatic response. Oxidative stress is an outcome of the acute inflammatory process at the lower respiratory airways, characterized by sharp changes in the arterial blood patterns. PaO 2 may reduce by as much as 50 mmHg within a very short time, while the blood pH may experience peak level of as high as 7.60 ( Graham & Eid, 2015).
Proper diagnosis of asthma is specific and follows the pathophysiological pattern and exacerbation of the condition. An allergy test may be preferred as the primary approach for the diagnosis. The patient’s medical history and family medical history is necessary to ascertain the past medical conditions about asthma (Price et al., 2015). Breathing tests and lung compliance evaluations are performed to determine the functionality of the patient’s lungs. Body fluids are evaluated for the presence of toxic substances, i.e., metal toxicity. Microbiological tests are conducted to determine the presence of chlamydia and viral load in blood. These laboratory and epistemological evaluations are necessary to formulate an effective evidence-based treatment plan. There are no specific medications for asthma. Medications that neutralize the trigger factors are recommended to curtail the commencement of the pathophysiological processes of asthma. These medications include antihistamines to prevent allergic reactions. Albuterol, Symbicort, adrenaline, and nebulizers are given in the ER with corticosteroids sometimes given.
Lastly, smoking causes an exacerbation of asthma by triggering pathophysiological mechanism that leads to acute or chronic inflammation and obstruction of the airways. The changes in airway result in a ventilation-perfusion mismatch which results in alteration of the arterial blood patterns. The determination of the exact mechanisms involved is important for proper diagnosis and effective treatment of the condition.
References
Graham, L. M., & Eid, N. (2015). The impact of asthma exacerbations and preventive strategies. Current medical research and opinion , 31 (4), 825-835. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25530129
Kumar, R. K., Herbert, C., & Foster, P. S. (2016). Mouse models of acute exacerbations of allergic asthma. Respirology , 21 (5), 842-849. Retrieved from https://onlinelibrary.wiley.com/doi/pdf/10.1111/resp.12760
Pola-Bibian, B., Dominguez-Ortega, J., Vilà-Nadal, G., Entrala, A., González-Cavero, L., Barranco, P., ... & Quirce, S. (2016). Asthma exacerbations in a tertiary hospital: clinical features, triggers, and risk factors for hospitalization. Journal of investigational allergology & clinical immunology , 0-0. Retrieved from http://www.jiaci.org/revistas/vol27issue4_4.pdf
Price, D., Harrow, B., Small, M., Pike, J., & Higgins, V. (2015). Establishing the relationship of inhaler satisfaction, treatment adherence, and patient outcomes: a prospective, real-world, cross-sectional survey of US adult asthma patients and physicians. World Allergy Organization Journal , 8 (1), 1. Retrieved from https://waojournal.biomedcentral.com/articles/10.1186/s40413-015-0075-y
Sears, M. R. (2015). Smoking, asthma, chronic airflow obstruction and COPD. European Respiratory Journal 45 : 586-588; DOI: 10.1183/09031936.00231414. Retrieved from http://erj.ersjournals.com/content/erj/45/3/586.full.pdf
Wark, P. A. B., & Gibson, P. G. (2006). Asthma exacerbations · 3:Pathogenesis. Thorax , 61 (10), 909–915. Retrieved from http://doi.org/10.1136/thx.2005.045187 .
