Pathophysiology behind the bronchoconstriction, airway hyper-responsiveness and airway obstruction in asthma
Jackson smith is an 18 years old male, having a history of asthma and who had been admitted in to the ED with severe breathlessness. The signs and the symptoms of asthma involves productive cough, chest tightness,, acute airway obstruction due to the narrowing of the airway and the formation of the mucus plugs and wheezing due to the narrowing of the airways.
The underlying pathophysiology behind the bronchoconstriction, airway hyper- responsiveness and airway obstruction is the inflammation in the airways causing several anatomical modifications in the airways (Brannan & Lougheed, 2012). The constriction is mainly due to the contraction of the bronchial smooth muscle in response to a variety of allergens.
Allergen induced bronchoconstriction is brought by the release of the IgE dependant mediators from the mast cells which includes prostaglandins, leukotriene, histamines and tryptase that contracts the muscles of the airways (Bonini & Usmani, 2015). Obstruction of the airways gives rise to sounds of wheezing limiting the flow of air through the airways. This is the main cause of the symptom of chest tightness in Mr. Smith. Wheezing is a kind of musical sound that that is produced due to the limited airflow through the airways (Melen & Pershagen, 2012).
Airway remodelling is the permanent changes that might occur due to inflammation. Hypertrophy and hyperplasia of the airway smooth muscles can cause this change in the airways and can be related to the progressive loss of the lung function that cannot be reversible by the current therapy (Brannan & Lougheed, 2012). Furthermore the regulation, repair and the remodelling process is still not well established. Airway hyper-responsiveness is also caused due to inflammation, dysfunctional neuro-regulation and the structural changes.
The vital signs of Jackson Smith displays that he had a low oxygen saturation level, which is a common symptom during an asthmatic attack. Low oxygen saturation can be related to fact that less amount of oxygen reaches the blood for being carried to the cells. Acute dyspnoea is also a common manifestation during the asthma exacerbations.
Jackson Smith was also found to be suffering from acute dyspnoea that is chest tightness that was preventing him to talk. The intensity of the dyspnoea depends upon the severity of the asthma, bronchoconstriction, dynamic hyperinflation, respiratory drive and other physiological factors (Antoniu, 2010). According to a study Antoniu, (2010) chest tightness was found to be associated with the mild bronchoconstriction and is attributed to the vagal stimulation due to the increased resistance of the airways but not to the hyperinflation. The respiratory rate of Mr. Smith was also found to be higher than the normal range, which implies that the person has to take more breaths to meet the oxygen demand.
Signs and symptoms of asthma such as chest tightness, wheezing, and low oxygen saturation level
A diminished breath sound in asthma manifests the fluid or air accumulation round the lungs or the thickening of chest walls, over inflation of the parts of the lungs or lessened flow of the air flow in to the lungs (Melen & Pershagen, 2012). The chest x-ray displayed a hyper-inflated lungs in asthmatic patients. Lung hyperinflation can be caused by the blockage of the airway that resists the expulsion air from the lungs. However lung hyperinflation is more common for the COPD patients and mild or moderate hyperinflation in the asthmatic patients. A rise in the serum lactate levels can be found in the asthma patients (Melen & Pershagen, 2012). This is due to the fact that when the oxygen level is low in the blood, the carbohydrate breaks down for producing energy with a subsequent production of lactic acid. As a result the lactate levels in the blood gets higher. Again it has been noticed that the administration of the Beta – agonist during the asthma treatment can also cause an abrupt increase the concentration of the lactate in the blood (Rodrigo, 2014). Finally, the rapid pulse rate of Jackson Smith is mainly due to the fact that the heart has to pump more quickly for sending blood to different parts of the body due to the less oxygen concentration. Some psychological factors comes in to play during asthmatic attacks that can be responsible for the elevated pulse rate.
- One of priority intervention is to increase the oxygen saturation level of Jackson Smith. Since the oxygen saturation level of Jackson is not below 90 %, hence application of oxygen therapy might not be helpful. It is necessary to assess the exacerbation by monitoring the peak expiratory flow rates and forced expiratory volume as taken by the respiratory therapist. Helping Jackson Smith to do a pursed lip breathing might increase the oxygen saturation level.
- Rationale:Oxygen saturation refers to the fraction of the oxygen saturated haemoglobin relative to the total haemoglobin present in the blood. The peak flow measure enables a nurse to measure the airway obstruction and the severity of the exacerbations (Sue Jordan, 2011). Pursed lip breathing helps in increasing the oxygen saturation level by increasing the probability of the entry of oxygen in the lungs.
- Another priority nursing strategy is the effective clearance of the airways. In Jackson Smith it is necessary to clear the hyper-secreted mucus to get a clear airways. The interventions include assessment of the respiratory rhythm, depth and rate, assessing for any sort of colour change in nail beds, buccal mucosa and lips (Melen & Pershagen, 2012). A nurse should assess the effectiveness of cough as coughing is the natural way of clearing secretion from the throat.
- Rationale: Assessment of the respiratory rate is necessary as it helps to determine any signs of impending respiratory distress. Assessing the nail and the lip colour might help to assess the presence of cyanosis that might indicate low oxygenation in the blood (Melen & Pershagen, 2012). Effective coughing is important as mucus plugs, thick secretions and respiratory muscle fatigue are due to ineffective cough.
Nebulised Salbutamol- It works on the β2-adrenoreceptors situated on the smooth muscles of the bronchi and stabilizes the receptor to its active state. More cAMP is generated as the receptors remains in the active state. This generation of the cAMP activates the intercellular cascade reducing the intracellular Ca2+, thus preventing the contraction of the smooth muscles of the airways.
Nebulised Ipratropium- Ipratropium acts as an anticholinergic agent blocking the muscarinic receptors of the acetyl choline and also helps to restrict the vagally mediated reflexes caused by the antagonisation of the acetyl choline receptors released by the vagus nerves. The anticholinergic action of the Ipratropium inhibits the effect of the cholinergic nerves inhibiting smooth muscle contraction (Morales et al., 2012).
Hydrocortisone-It inhibits the release of the secreatagogue by the macrophages, thus reducing the excessive secretion of the mucus in to the airways. It stops the late phase reaction by inhibiting the chemotaxis and inflammatory response (Alangari, 2014).
- b) Careful surveillance of the arterial blood gases and the vital signs are necessary after providing salbutamol to the patients. Dosage for the Salbutamol should be restricted to 5mg. It is necessary to consider if the patient has history of hypersensitivity. Cardiac dysrhythmias and tachycardia should be monitored. The patient should be assessed for mild tachycardia, hypokalemia and nervousness. Before the application of the ipratropium, it is necessary to adjust the dosage as per the body weight of the patient (Melani et al., 2012). A mouthpiece can be used for the administration of the inhalers (Cates, Welsh & Rowe, 2013). Nurses should be able to assess any signs of dizziness, tremors or shaking after the application of the medicine.
Before administering hydrocortisone, the nurses should check on the vital signs and should be mindful about how long the medicines will be continued as hydrocortisone can cause long-term effects such as hypertension and peptic ulcer diseases (Alangari, 2014).
References
Alangari, A. A. (2014). Corticosteroids in the treatment of acute asthma. Annals of Thoracic Medicine, 9(4), 187–192. https://doi.org/10.4103/1817-1737.140120
Antoniu, S. A. (2010). Descriptors of dyspnea in obstructive lung diseases. Multidisciplinary respiratory medicine, 5(3), 216.
Bonini, M., & Usmani, O. S. (2015). The role of the small airways in the pathophysiology of asthma and chronic obstructive pulmonary disease. Therapeutic advances in respiratory disease, 9(6), 281-293. https://doi.org/10.1177/1753465815588064
Brannan, J. D., & Lougheed, M. D. (2012). Airway Hyperresponsiveness in Asthma: Mechanisms, Clinical Significance, and Treatment. Frontiers in Physiology, 3, 460. https://doi.org/10.3389/fphys.2012.00460
Cates, C. J., Welsh, E. J., & Rowe, B. H. (2013). Holding chambers (spacers) versus nebulisers for beta?agonist treatment of acute asthma. The Cochrane Library. https://dx.doi.org/10.1136/thoraxjnl-2012-202071
Melani, A. S., Canessa, P., Coloretti, I., DeAngelis, G., DeTullio, R., Del Donno, M., … & Vaghi, A. (2012). Inhaler mishandling is very common in patients with chronic airflow obstruction and long-term home nebuliser use. Respiratory medicine, 106(5), 668-676. https://doi.org/10.1016/j.rmed.2011.11.016
Melen, E., & Pershagen, G. (2012). Pathophysiology of asthma: lessons from genetic research with particular focus on severe asthma. Journal of internal medicine, 272(2), 108-120. https://doi.org/10.1111/j.1365-2796.2012.02555.x
Morales, D. R., Jackson, C., Fielding, S., & Guthrie, B. (2013). Long-acting β-agonist prescribing in people with asthma in primary care. Thorax, 68(2), 192-194.
Rodrigo, G. J. (2014). Serum lactate increase during acute asthma treatment: a new piece of the puzzle. Chest, 145(1), 6-7. DOI: https://doi.org/10.1378/chest.13-2042
Sue Jordan, M. B. (2011). Bronchodilators: implications for nursing practice. DOI 10.7748/ns2011.03.15.27.45.c2999
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