Pathogenesis of Severe Acute Asthma: Understanding the Mechanisms and Nursing Priorities
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This article discusses the pathogenesis of severe acute asthma, including its mechanisms and nursing priorities for patients. It covers pharmacological therapy, drugs administered, and monitoring of the drugs.
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Pathogenesis ofAcute Severe Asthma Severe acute asthmareflects a severe exacerbation which doesn’t respond to normal treatment process by use of bronchodilators and corticosteroids drugs. Basic symptoms include having a tight chest, shortness of breath, cough which is dry, labored breathing and excess wheezing. It usually presents itself as a life-threatening condition which often calls for emergency attention, (Cook & Saglani, 2016). Asthma inflammation of eosinophils occurs in the early phase and mixes itself with cellular infiltrate which is composed of eosinophils, lymphocytes cells, neutrophils, and mast cells. Allergic inflammation often begins with the progression of the predominant helper T 2 lymphocyte which is carried away contrary to a T1 lymphocyte. This allows for allergen exposure within the genetically susceptible individual. Specific exposure to allergens with the influence of helper T Cells which often leads to B-Lymphocyte reflects an elaboration of immunoglobin and antibodies which are specific for the allergen. Subsequent allergen exposure often leads to cross bridges in the IgE molecules and leads to activation and releasing an array of mediators. The mediators, in this case, are the leukotrienes, histamine, C4, D4 and E4 with the host cytokines. These mediators often lead to bronchial smooth constriction of the muscles, vascular leakage, and cell inflammation. The process often leads to obstruction of the smooth muscles, airway edema, inflammatory cells influx and production of intraluminal mucus. The airway inflammation can cause hyperactivity in the characteristic of asthma. Severe airway obstruction leads to impaired gas exchange which results in gas exchange and low oxygen levels, (Leatherman, 2015). Airflow decline in the asthmatic state is caused by a variety of factors and changes in the air airway; these factors include; Bronchi constriction The common symptom of asthma is the airway narrowing which leads to interference of airflow. In severe acute of asthma, the bronchial smooth contraction which leads to narrowing of airflow. Bronchi constriction induced by allergens often originates from IgE dependent mediators released from mast cells which include tryptase, leukotrienes, histamines, and prostaglandins which have a direct effect on the airway. Drugs can be a factor in the constriction of the airways, (Puranik, Forno, Bush & Celedon,2017). Aspirin and other related nonsteroidal drugs have been shown to have an effect on the narrowing of the bronchioles. Airway Edema and hyperresponsiveness When the disease becomes persistent with progressive inflammation, other factors may 3
have limited airflow. These factors include edema, hypersecretion of mucus, inflammation and the formation of mucus inspected plugs and also the structural changes occurring in the hypertrophy. On the other hand, airway hyperresponsiveness is an execrated bronchi constrictor response leading to a wide variety of stimuli. Often the degree of airway hyperresponsiveness is characterized by the intractable responses to difficulties with methacholine, (Danek et al., 2017). The underlying mechanisms often influencing hyper-responsiveness are many and can include neuro regulation and structural changes. Airway remodeling Lastly, airway remodeling in severe acute asthma can be a partial problem which is reversible. Structural changes can occur in the airway. They lead to structural changes in the lungs. This repair and regulation of the airway are likely to have an influence on the nature of asthma attack, (Witt et al., 2014). Nursing priorities for the patient Pharmacological therapy High priority nursing intervention for the patient is undertaking pharmacological administration therapy. Treatment protocol for the patient needs to be based on the degree of airflow administration on the airflow obstruction. Drug management for the patient entails offering rapid acting inhalation of Beta 2 adrenergic bronchodilators as the first line treatment process. Further, the bronchodilators will be administered through inhalation and offering the patient a pressurized metered dose inhaler having a valved holding chamber. The mixture use of treatment of short-acting anticholinergic and the beta 2 adrenergic bronchi dilators is effective for this patient. Further small doses of inhalation of corticosteroids are effective for this patient, (Lefebvre et al., 2015). Management of respiratory status Management of the respiratory status for the patient is critical. The patient’s partial pressure for oxygen and carbon dioxide is below the recommended standards. Thus there is a need for managing the respiratory distress for the patient. Increase in ventilation of the airflow is paramount. With shortness of breath, there is a need to administer oxygen so as to maintain oxygen saturation of 92% and above. This is in order to eliminate the carbon dioxide and the alkalemia. Further increasing the lung volume is crucial and the static pressure is shifted up. This improvement of the airway is usually reversible after administration of beta-agonists and the administration of anti-inflammatory agents, (Bayes & 4
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Thomson, 2016). Drugs administered to the patient Nebulised Salbutamol Nebulizer salbutamol is an inhaled aerosol which acts on the β2adrenoreceptors affecting the smooth muscle which envelops the bronchi. The drug binds non-covalently the epinephrine active site, this offers stability to the receptor in the active state. The receptor further gets more time in its form which allows the formation of more cAMP. This triggers cascades on the intracellular releasing potassium ions and lowers the level of free intracellular calcium ions, hindering the ability of the muscles to contract. Once the binding is done the salbutamol is carried in the body through the blood and attacks the β2receptors before its inactivation, (Neame et al., 2015). Ipratropium bromide This is a synthetic compound of ammonia which has a similar structure of atropine and function as a bronchodilator. It is effective in the management of cholinergic mediated bronchospasm, which is associated with the chronic obstructive pulmonary disease. This drug functions as an anticholinergic agent, acting by blocking the muonic receptors of cholinergic without the subtypes specification. This leads to a decline in cyclic guanosine monophosphate. Due to this action of cGMP in the calcium intracellular, it leads to a decline in the contraction of the smooth muscle, (Memon, Parkash, Khan, Gowa & Bai, 2016). IV Hydrocortisone Hydrocortisone is able to bind the systolic glucocorticoid receptors. When the binding is done, it forms the receptor-ligand complex undergoes translocation into the cell nucleus, where the glucocorticoid response elements are. The bound receptor of the DNA binds itself interacts itself to the basic transcription factors. This leads to an increase in expression of corticosteroids actions which involve lipoproteins, inhibitory proteins, controlling prostaglandin synthesis and the leukotrienes. Glucocorticoid leads to inducement of the lipocortin synthesis, which offers to bind to the cell membranes thus preventing phospholipase from the substrate arachidonic acid. Glucocorticoids further offer stimulation of the lipocortin -1 which escapes to the extracellular space binding to the leukocyte membranes which eventually binds various inflammatory events such as those causing asthma conditions, (Mukenji et al, 2015). Monitoring of the drugs administered Administering of Nebulised Salbutamol needs to be used with the right nebulizer 5
through a face mask. This drug is used in cases whereby there is chronic bronchospasm which is not responding to regular convention treatment methods, thus care needs to be taken. Usual dosage among adults is 2.5mg per dose however this can be increased and repeated severally in a day. Higher doses of upto 40mg per day can be offered to patients. Intake of Ipratropium bromide is usually 2 inhalations equivalent to 36mcg and should not exceed 12 inhalations in duration of 24 hours equivalent o 500mcg. Monitoring of drug reaction is key in this process. The patient needs to be monitored for any hypersensitivity incase for those who have allergies to soy, lecithin and other food derivatives. IV Hydrocortisone administration to the patient needs to be monitored through testing and checking for any side effects and assessing response of the therapy to the patient. Thus taking the required dosage is recommended for any patient. 6
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Memon, B. N., Parkash, A., Khan, K. M. A., Gowa, M. A., & Bai, C. (2016). Response to nebulized salbutamol versus combination with ipratropium bromide in children with acute severe asthma.JPMA. The Journal of the Pakistan Medical Association,66(3), 243-246. Mukerji, S., Shahpuri, B., Clayton-Smith, B., Smith, N., Armstrong, P., Hardy, M., ... & Marsh, E. (2015). Intravenous magnesium sulphate as an adjuvant therapy in acute exacerbations of chronic obstructive pulmonary disease: a single centre, randomised, double-blinded, parallel group, placebo-controlled trial: a pilot study.NZ Med J,128, 34-42. Puranik, S., Forno, E., Bush, A., & Celedón, J. C. (2017). Predicting severe asthma exacerbations in children.American journal of respiratory and critical care medicine, 195(7), 854-859. 8