Pathogenesis of Severe Acute Asthma: Understanding the Mechanisms and Nursing Priorities

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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Severe Acute Asthma; concept map
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Pathogenesis of Acute Severe Asthma
Severe acute asthma reflects 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
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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 &
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Thomson, 2016).
Drugs administered to the patient
Nebulised Salbutamol
Nebulizer salbutamol is an inhaled aerosol which acts on the β2 adrenoreceptors
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 β2 receptors
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
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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.
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References
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