Asthma is a chronic inflammatory condition that affects the airways. It is characterized by tracheobronchial tree hyper-responsiveness to specific stimuli. Exposure to such stimuli triggers reversible airway obstruction. Advanced practice nurses should understand the pearls of asthma management. Importantly, patients should be helped to identify the triggers of their symptoms to avoid exacerbations. Asthma symptoms may be acute or chronic. These two forms of the disease have different pathophysiological mechanisms. An individual's age may also influence the disease process in asthma. Further, age may influence the diagnosis and treatment of the condition.
Chronic Asthma
The pathogenesis of chronic or persistent asthma is two-fold. The first phase is characterized by an early asthmatic response while the second phase is a delayed response. During the initial response, exposure of the bronchial mucosa to antigens results in the activation of dendritic cells in the lungs. These antigen-presenting macrophages present the trigger antigens to T-helper (Th) cells. Consequently, the differentiation of the Th cells into Th2 cells occurs. This change is followed by the production of pro-inflammatory cytokines and interleukins. The release of these mediators results in the activation of eosinophils and B cells (Huether & McCance, 2017). On activation, the B cells produce antigen-specific antibodies (IgE). The immunoglobulin then attaches to the surfaces of mast cells. The successive cross-linkage of the IgE with the antigen precipitates mast cell degranulation and discharge of pro-inflammatory mediators (Huether & McCance, 2017). Resultantly, capillaries in the tracheobronchial tree dilate and their permeability increases. With time, mucosal edema, bronchospasms, and mucus hyper-secretion ensue leading to airway narrowing. Eosinophils exert direct tissue injury and release neuropeptides that amplify bronchial hyper-responsiveness.
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The delayed reaction occurs about eight hours following the outset of the initial phase (Huether & McCance, 2017). During the acute phase, eosinophils, neutrophils, and lymphocytes are recruited chemotactically. This recruitment explains the latent release of pro-inflammatory mediators during the delayed response and the worsening of mucus secretion, bronchospasms, and edema. Consequently, airflow is impeded. The eosinophil-mediated direct cytotoxicity contributes to airway fibrosis. Gradually, the ciliated epithelial cells are destroyed causing the impairment of mucociliary functions. As a result, the mucus accumulates and the debris from cellular destruction blocks the airway compromising its patency. In the absence of treatment, airway remodeling occurs. Such alteration is typified by sub-epithelial fibrosis and the hypertrophy of smooth muscle (Huether & McCance, 2017).
Acute Asthma Exacerbation
Acute asthma exacerbations occur secondary to environmental exposure to triggers or allergens. Some of the most common triggers include bacterial endotoxins, viruses, and particulates (Gautier & Charpin, 2017) . These allergens elicit cytokine responses that culminate in the infiltration of the airways by granulocytes. Upon activation of the granulocytes oxidative stress ensues due to the increase in the production of reactive oxygen species. The production of these species overpowers the antioxidant mechanisms of the body leading to lipid and protein oxidation. Exacerbations are also characterized by rapid bronchoconstriction stemming from the IgE-dependent production of pro-inflammatory mediators following mast cell degranulation (Bradding & Arthur, 2016) . In acute exacerbations, the obstruction of airways obstructs airflow and reduction in flow rates.
Reduced expiratory flow causes air trapping, dyspnea, and hyperinflation distal to the obstruction. Airway obstruction and an increase in lung volume trigger hyperventilation. Consequently, hypoxemia with no CO 2 retention arises. This causes the stimulation of the respiratory center, hyperventilation, and resultant respiratory alkalosis (Vasileiadis et al., 2019) . The continued blockade of expiratory flow causes further air entrapment causing extensive expansion of the lungs and thorax. As such, tidal volume is decreased leading to CO 2 retention and respiratory acidosis (Vasileiadis et al., 2019) . Accordingly, the arterial blood gas picture during an exacerbation may be high or normal PaCO 2 , diminished PaO 2 , and low pH (Vasileiadis et al., 2019) . PaO 2 decreases based on the extent of obstruction. Importantly, increased PaCO 2 is an ominous sign.
Age and Asthma
Pathophysiology
Asthma phenotype may be influenced by age-dependent physiological alterations. According to Boulet (2016), airway obstruction is more pronounced in the elderly than in younger asthmatic individuals. A decline in lung function has also been associated with aging. As one ages, lung compliance and its elastic recoil decrease. Additionally, there is a decrease in respiratory muscle tone and a concurrent increase in closing and residual volumes (Boulet, 2016). Reportedly, children with asthma often present with intermittent symptoms apart from the few cases where daily symptoms manifest. Contrarily, asthma in adults typically presents with persistent symptoms. Comparatively, children are more likely to react to allergens (Boulet, 2016). In most cases, the symptoms in children may reduce or almost disappear during adolescence and reappear later in their lives. Children are also very sensitive to secondhand smoke and may visit the emergency department more frequently than adults (Boulet, 2016).
Diagnosis
The diagnostic approaches to asthma apply to persons of all ages The diagnosis of asthma is based on a compelling history of recurring episodes of difficulty in breathing and/or wheezing, as well as, confirmatory spirometry. Kasper et al. (2015) maintain that physical examination should also be conducted to single out the classic signs of asthma. Electrocardiography and radiological examination are often employed to rule out other causes of precipitants of wheezing (Kasper et al., 2015). Contingent on the assessment of a clinician bronchoprovocation testing may be conducted. Additionally, allergy testing could be carried out to determine the allergens that trigger the exacerbation of asthma symptoms in the patient (Kasper et al., 2015).
Treatment
Acute Asthma Exacerbation
In mild asthma exacerbation, a nebulized beta-2 (β2) agonist is used primarily for the management of symptoms in young children (Kumar & Clark, 2017) . Among older children and adults, metered-dose inhalers and spacers can be used. If the patient does not improve, three doses of nebulized β2 agonist at 20-minute intervals along with eight liters of oxygen should be given (Kumar & Clark, 2017) . These could be combined with ipratropium or oral steroids. If improvement is registered, the patient should be observed and discharged with a β2 agonist with or without oral steroids. Admission is indicated for severe cases. On admission, a nebulized β2 agonist should be administered every 20 minutes or continuously together with intravenous corticosteroids (Kumar & Clark, 2017) . Following improvement, further reviewing and continuous observation should be done. If the patient does not improve, intensive care, parenteral β2 agonist, and intravenous aminophylline should be considered.
Chronic Asthma
For sporadic intervallic asthma, intermittent administration of an inhaled β2 agonist is indicated (Kumar & Clark, 2017) . Frequent episodic cases warrant the introduction of inhaled sodium cromoglycate and the continuation of intermittent inhaled β2 agonists (Kumar & Clark, 2017) . For patients with persistent asthma, sodium cromoglycate is replaced with low-dose inhaled corticosteroids with the continuation of an inhaled β2 agonist. Progression of the disease necessitates the upward titration of the dose of inhaled corticosteroid to moderate levels with the continuation of the intermittent inhaled β2 agonist (Kumar & Clark, 2017) . Subsequently, if no improvement is registered, inhaled ipratropium, methylxanthines, or long-acting β2 agonists may be considered. In more advanced asthma, a high-dose inhaled corticosteroid is indicated. Long-term oral steroids may then be prescribed afterward (Kumar & Clark, 2017) .
References
Boulet, L. (2016). Asthma in the elderly patient. Asthma Research and Practice , 2 (1). doi: 10.1186/s40733-015-0015-1
Bradding, P., & Arthur, G. (2016). Mast cells in asthma - state of the art. Clinical & Experimental Allergy , 46 (2), 194-263. doi: 10.1111/cea.12675
Gautier, C., & Charpin, D. (2017). Environmental triggers and avoidance in the management of asthma. Journal of Asthma and Allergy , 10 , 47-56. doi: 10.2147/jaa.s121276
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Elsevier.
Kasper, D., Fauci, A., Hauser, S., Longo, D., Jameson, J., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th ed.). New York: McGraw-Hill Education.
Kumar, P., & Clark, M. (2017). Clinical medicine (9th ed.). London: Bailliere Tindall.
Vasileiadis, I., Alevrakis, E., Ampelioti, S., Vagionas, D., Rovina, N., & Koutsoukou, A. (2019). Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology. Journal of Clinical Medicine , 8 (4), 563. doi: 10.3390/jcm8040563
