Definition and etiology
Asthma is characterized by airway hyper responsiveness to normal stimuli, reversible airflow obstruction and variable airflow as show by Peak Expiratory Flow. Its pathogenesis involves both environmental and genetic factors. The later includes atopy, a positive family history of asthma and intolerance identified as polygenic. Gender and ethnicity also play a role at different stages of life (Ferreira, et al., 2017). Perfumes, pollen, dust, smoke from industries and car exhaust fumes have been identified as environmental factors that play a role in asthma progression. Dietary deficiency of vitamins C and E (antioxidants) have been shown to predispose to asthma. Pollution from indoors like dust, pets and pests are also triggers for asthma. (Maslan & Mims, 2014). Oral contraceptives and non-steroidal anti-inflammatory drugs like aspirin and diclofenac, when used for long can lead to one developing asthma. It is possible that Smith’s problem can be traced from the family, and accentuated by environmental factors. (Kumar, Abbas, & Aster, 2015). Environmental and genetic factors, when combined, produce an additive effect for asthma progression. The hall mark of the asthma is airway inflammation, edema of mucosa, bronchoconstriction, hypertrophy of smooth muscles of the bronchus and mucous gland (Lambrecht & Hammad, 2015)
Genetic susceptibility to asthma, an example of type 1 hypersensitivity reaction (atopy) plays an important role in development of asthma. Upon exposure to an offending agent, inflammation ensues (Craft et al, 2015.)Eosinophils and neutrophils are the major inflammatory cells recruited. In atopic asthma, TH2 production is too much. It fuels production of IL-4 which in turn stimulates production of IgE (produced by B cells). B cells are activated by IL-13 which also stimulates mucous production (Craft et al, 2015). IL-5 activates eosinophils. Degranulation happens when IgE coats mast cells, making the membrane become unstable and release inflammatory cytokines, initiating early and late responses of asthma. Increased mucus production, vasodilation and bronchoconstriction mediated by vagal stimulation in the epithelium is characteristic of an early wave (Lambrecht & Hammad, 2015). Eosinophils, neutrophils and T cells are activated in the late phase. Continuous chemotaxis and activation of TH2 cells amplify the reaction. (Kumar, Abbas & Aster, 2013). Repeated exposure to allergen causes airway remodeling that has hypertrophied muscles and mucous glands that makes the airway narrow (Craft et al, 2015).
Jackson Smith presents with Acute Severe Asthma (ASA) that is usually unresponsive to corticosteroid and bronchodilator therapy. Severe dyspnea is due to airway hyperactivity to an allergen causing inflammation and increased mucus production that limit amount of air entry and outflow (Kumar, Abbas & Aster, 2013).Airway remodeling is also a causative factor. Narrowing of lumen causes increased respiratory effort to deliver more oxygen and wash out carbon dioxide Respiratory center is sensitized by excess carbon dioxide (as Jackson Smith’s) to wash out excess CO2. Oxygen saturation at room air was low in Smith’s case because of inadequate oxygen delivery to blood by narrowed lumen of bronchi.
Pathogenesis
The body’s response for low oxygen tension in tissues is through increasing the blood pressure and heart rate so that more blood with oxygen can be delivered per unit time. Asthma attack leaves a patient with inadequate oxygen in tissues, causing blood to be redirected to other vital organs like brain and heart (Craft et al, 2015). Smith’s blood pressure and pulse rate were increased so that more oxygen can be delivered in tissues per unit time, as part of physiological body response. Physical examination, including auscultation revealed widespread wheeze and reduced air entry in lungs. Narrowing of bronchi is responsible for reduced air entry and exit thus the finding on auscultation. Wheeze is explained by air turbulence as it rushes in the narrowed lumen of the bronchi. Hyperinflation of lung fields on chest X-ray is due to chronic air trapping in lungs (Pijnenburg, et al., 2015).
Blood gas analysis performed on Smith shows abnormal values. There is renal compensation of respiratory acidosis as shown by high PaCO2 of 50 mmHg (Normal is 35-45 mmHg) (Pijnenburg, et al., 2015). This is evident of long time respiratory distress. Asthma makes the patient inhale inadequate oxygen and makes exhalation of carbon dioxide incomplete therefore accumulating excess carbon dioxide. When excess carbon dioxide dissolves in blood, weak carbonic acid is formed, hall mark for respiratory acidosis. Weak carbonic acid further degrades to hydrogen ions as shown by Magge, Pascanu & Salerno, (2017). Excess hydrogen ions is buffered by bicarbonate ions. The kidneys increases absorption of bicarbonate ions to buffer the low pH. Patients hyperventilate in acute states of respiratory distress, a process leading to respiratory compensation of respiratory acidosis as shown by National Asthma Council Australia, (2017).
Two high priority interventions that should be undertaken by nurses to manage Smith’s ASA are bronchodilator therapy initiation and oxygen administration. Severity of the attack can also be assessed as described in by the National Asthma Council Australia, (2017).
Salbutamol, 12 puffs equivalent to 100 mcg per actuation using pressurized metered dose inhaler (pMDI) and a spacer is the desired bronchodilator therapy (National Asthma Council Australia, 2017). 5mg of salbutamol in a nebulizer is used in cases where the patient cannot breathe. Oxygen, via a high pressure flow (venturi) system should be given targeting a saturation of above 94% in young patients like Smith (National Asthma Council Australia, 2017).
Assessing patient’s condition while giving bronchodilator and oxygen therapy is necessary. Repeat doses of salbutamol (3 doses in 1 hour) or in PRN form should be initiated. Ipratropium bromide, 8 puffs through pMDI or 500 mcg nebule added to salbutamol is added in cases of poor response. 37.5-50 mg oral prednisolone, a systemic corticosteroid (for 5 days) or 100 mg of intravenous hydrocortisone every 6 hours is also given to slow down inflammation (National Asthma Council Australia, 2017). Therapy response is reviewed after a week and recorded (National Asthma Council Australia, 2017). A step down therapy started if a good control has been achieved. Calculation of Smith’s minimum dose of drug is also done and during this period, symptoms and peak expiratory flow rate is monitored then a follow up visit scheduled (Aitken, Marshall, & Chaboyer, 2015). Drug shelf life is also checked to make sure it is still viable.
Signs and symptoms
Ipratropium is a short acting anti muscarinic drug that has competitive binding properties to cholinergic receptors of bronchial smooth muscles. It blocks acetylcholine therefore inhibiting bronchoconstriction. Vasodilation and bronchodilation is the ultimate effect of inhibition of vagal stimulation in sub epithelium (FitzGerald et al., 2018).
Salbutamol acts via the G-protein coupled pathway. It is a short acting beta 2 agonist. cAMP and protein kinase A is activated upon stimulation of G protein (Carotenuto, Perfetti, Calcagno, & Meriggi, 2018). There is activation of myosin light chain phosphatase that enables entry of calcium via gated ion channels causing smooth muscle relaxation. This causes bronchodilation.
Intravenous hydrocortisone is a systemic corticosteroid (Radojicic, Keenan, & Stewart, 2016). It works by inhibiting inflammatory path in asthma by blocking phospholipase A2 that supressesLipocortin-1. Phospholipase A2, when blocked will lead to depletion of eicosanoids. Therefore inflammatory cells recruitment is suppressed (Kumar, Abbas & Aster, 2013).
Monitoring for therapeutic effects of ipratropium bromide, hydrocortisone and salbutamol is one of the nursing implications (Johnson, 2017). Patient improvement and side effects should also be monitored. For instance, low potassium levels and tachycardia after salbutamol use (especially in overdose) , dry mucous membrane, urinary retention and slow heart rate for ipratropium bromide and glucose intolerance, infections susceptibility and weight gain in prolonged use of hydrocortisone should be looked into. Liver and renal function tests should be monitored. Correct route, dosage and shelf life of the drug should also be looked into when the patient is not responding to therapy (Ojo et al., 2014).
References
Aitken, L., Marshall, A. & Chaboyer, W. (2015). ACCCN’s critical care nursing (3rd ed.). Chatswood, NSW: Elsevier Australia. Chapter 10.
Craft, J.A., Gordon, C.J., Huether, S.E., McCance, K.L., Brashers, V.L. & Rote, N.E. (2015). Understanding pathophysiology – ANZ adaptation (2nd ed.). Chatswood, NSW: Elsevier Australia. Chapter 24 & 25.
Ferreira, M. A., Jansen, R., Willemsen, G., Penninx, B., Bain, L. M., Vicente, C. T., & Baltic, S. (2017). Gene-based analysis of regulatory variants identifies 4 putative novel asthma risk genes related to nucleotide synthesis and signaling. Journal of Allergy and Clinical Immunology, 139(4), 1148-1157.
Johnson, R. A. (2017). A Quick Reference on Respiratory Acidosis. Veterinary Clinics: Small Animal Practice, 47(2), 185-189.
Kumar, V., Abbas, A., & Aster, J. (2013). Robbins Basic Pathology (9th ed., pp. 468-470). Canada: Elsevier Saunders.
Lambrecht, B. N., & Hammad, H. (2015). The immunology of asthma. Nature immunology, 16(1), 45.
Magge, A., Pascanu, R., & Salerno, E. (2017). C58 CRITICAL CARE CASE REPORTS: NOTABLE CAUSES AND COMPLICATIONS IN ACUTE RESPIRATORY FAILURE: Extracorporeal Membrane Oxygenation in Patients with Acute Severe Asthma. American Journal of Respiratory and Critical Care Medicine, 195.
Maslan, J., & Mims, J. W. (2014). What is asthma? Pathophysiology, demographics, and health care costs. Otolaryngologic Clinics of North America, 47(1), 13-22.
National Asthma Council Australia. (2017) Australian Asthma Handbook – Quick Reference Guide, Version 1.3. National Asthma Council Australia, Melbourne. Available from: https://www.asthmahandbook.org.au
Ojo, O. O., Basu, S., Jha, A., Ryu, M., Schwartz, J., Doeing, D., … & Halayko, A. J. (2014). D29 MOLECULAR SIGNALS AND CELLULAR MECHANICS: FOCUS ON ASTHMA: S100a8/a9 Is A Mediator Of Asthma Pathophysiology In An Acute Allergic Model Of Asthma. American Journal of Respiratory and Critical Care Medicine, 189, 1.
Pijnenburg, M. W., Baraldi, E., Brand, P. L., Carlsen, K. H., Eber, E., Frischer, T., … & Mantzouranis, E. (2015). Monitoring asthma in children. European respiratory journal, 45(4), 906-925.
Radojicic, D., Keenan, C. R., & Stewart, A. G. (2016). The Physiological Glucocorticoid (GC), Hydrocortisone, Limits Selected Actions Of Synthetic GC In Human Airway Epithelium. In A40. EPITHELIAL REGULATION OF INFLAMMATION (pp. A1472-A1472). American Thoracic Society.
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