Acute Severe Asthma: Pathogenesis, Clinical Manifestations, and Nursing Strategies

Running head: ACUTE SEVERE ASTHMA 1
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Acute Severe Asthma 2
Concept map
Figure 1: Concept map showing the causes, pathogenesis, clinical manifestation, diagnostic
procedures, management, prognosis and prevention of Acute Severe Asthma
Question 1: Pathogenesis and clinical manifestations explained
Asthma is an airway disease, characterized by its chronicity. The hallmark of asthma is
airway hypersensitivity to normal environmental allergens, reversible airflow and a variable
course of airway obstruction (Maslan & Mims, 2014.) Asthma’s pathogenesis involves
environmental and genetic factors. Environmental factors involve exposure to allergens like
pollen, dust and perfumes. Other aspects are housing conditions like cooking using firewood,
poor ventilation and presence of pets like cats in the house. Non-environmental factors not
including genetics include diet and drugs. Drugs like aspirin and oral contraceptives have been
shown to predispose one to asthma (Ojo et al., 2014). Diets low in anti-oxidants like Vitamin E

Acute Severe Asthma 3
and Vitamin C has also been associated with developing asthma. Genetic factors like atopy,
gender and ethnicity have been implicated to enhance progression of asthma. Others include
positive family history of asthma and polygenic intolerance.
In Jackson’s case, asthma attack can be traced back to positive family history and atopy.
This may have been triggered by an allergen. It is therefore correct to say that both genetic and
environmental factors may have played a role in Smith’s asthma attack. The two factors
combined cause airway remodeling especially in repeated exposure to an allergen (Ojo et al.,
2014).
The major etiological agent for asthma is attributed to genetic predisposition that induces
a type 1 hypersensitive reaction. Numerous inflammatory cells and interleukins play a role in the
cascade. Inflammatory cells involved are neutrophils and eosinophils. Atopic patient
demonstrates a high level of TH2 cells production. (Ojo et al., 2014).These cells stimulate
production of interleukin 4 (IL-4) that promotes the release of IgE. B cells are also responsible
for production of IgE. These B cells are usually activated by IL-13 which also oversees
production of mucus in the bronchial smooth muscles as described by Chung, (2015).
Eosinophils are usually activated by IL-5. Upon exposure to an allergen, the IgE coats mast cells
and cause degranulation to release histamine.
An early and late wave of reactions have been documented. The former is evident during
the degranulation phase of mast cells. Early wave has bronchus constriction, marked mucus
production and variable vasodilation (Lougaris et al., 2017). Epithelial vagal receptors mediate
bronchoconstriction. T-cell, eosinophil and neutrophil activation caused by inflammation is
characteristic of late phase. Airway remodeling occur when there is repeated exposure to

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allergen. This included bronchial smooth muscle hypertrophy, hypertrophy of mucus gland,
vascularization and collagen deposition in sub epithelium (Craft et al, 2015).
One of the findings was that Smith had an increased blood pressure and heart rate. This
was a physiological response to increase oxygen delivery to tissues at a time. Physical
examination also revealed reduced breath sounds and wheeze. Wheeze was experienced due to
narrowed bronchial lumen that caused turbulent flow of air as it rushed through a narrow space.
Breath sounds were reduced on auscultation because air entry was limited as a result of
narrowing of bronchial muscles (Kumar, Abbas & Aster, 2013).
Arterial blood gas showed compensated respiratory acidosis (renal compensation). This is
shown by high partial pressures of carbon dioxide at 50 mmHg. This is suggestive of long
respiratory distress as described by a book VENTILATOR, (2016). When carbon dioxide is in
excess in blood, it dissolves to form weak carbonic acid that disintegrates to release hydrogen
ions that lowers the blood pH. Short term solution for this is increased respiratory effort to wash
out the excess carbon dioxide. This is why his respiratory rate was high (at 32 breaths per
minute). Long term solution for respiratory acidosis is renal compensation. In this case, there is
increased absorption of bicarbonate ions by the kidneys to act as a buffer (Johnson, 2017).
Smith’s also presents with severe dyspnea. This is because of acute excercubation of
asthma (ASA). ASA does not respond to standard treatment with bronchodilators and
corticosteroids. Dyspnea is due to airway obstruction that is overseen by increased mucus
production as a result of hypertrophy of mucus glands. Airway narrowing is also contributed by
bronchoconstriction secondary to inflammation and airway narrowing due to remodeling that
results into hypertrophy of bronchial smooth muscles VENTILATOR, (2016). These three
factors result into reduced air entry making the patient dyspneic. As a result, there is increased