Asthma is an inflammatory disorder of the airways resulting from an immune response to allergens
or triggers, causing inflammation and bronchoconstriction( Burchum&Rosenthal,2022).Peter was
diagnosed with asthma when he was three years old. This diagnosis suggests that he has a history of
airway hyperresponsiveness and inflammation, which puts him at a greater risk for acute asthma
exacerbations. Therefore, mild trigger factors like allergens or respiratory infections, could trigger an
acute inflammatory response in Peters' airways and cause intense bronchoconstriction. As a result,
his airways become constricted and narrow, which leads to increased resistance in airflow and
excessive mucus production. This has caused Peter to experience various clinical symptoms, such as
tachypnoea, hypoxia, and hypoxemia; using accessory muscles; and respiratory acidosis, wheezing,
And hyperinflation of the lungs (Barnes,2018) The pathophysiology of acute exacerbations of
Asthma involves the binding of allergens to dendritic cells, which are specialised macrophages in the
airway epithelium. These cells play a role in engulfing microorganisms and activating CD4TH2 helper
cells. The release of chemical mediators known as interleukins by these helper cells stimulates two
types of immune cells: plasma cells and eosinophils.
Eosinophils release inflammatory mediators such as cytokines and leukotrienes, while plasma cells
activate mast cells through IgE-mediated activity using immunoglobulin E. This binding process leads
to mast cell degranulation, resulting in the release of toxic granules that contain strong inflammatory
mediators like histamine, leukotriene, and prostaglandins.Ultimately, this cascade of events leads to
an increase in inflammatory mediators within the patient's system (Craft et al., 2019) This excess of
inflammatory mediators causes mucosal inflammation. Consequently, the mucosal lumen, the
empty passage through which air enters the lung, becomes narrow or constricted due to mucosal cell
oedema. This limited passage results in a wheeze-like whistling as air tries to force its way through
the obstruction. During episodes of acute asthma exacerbations. Inflammation occurs in the alveoli
and capillary cells. This inflammation limits the exchange of gases, leading to reduced diffusion of
oxygen and carbon dioxide. Consequently, hypoxemia occurs, which is characterised by a decrease in
the amount of oxygen present in the blood and a diminished ability for oxygen to reach the organs'
tissues, resulting in tissue-level hypoxia. Additionally, inadequate ventilation in lung segments due to
mucosal secretion and edoema further compounds the issue by causing poor ventilation. As a result,
this alters the overall ventilation perfusion ratio and leads to a V/Q mismatch. Due to limitations in
the airways, the oxygen partial pressure decreases in arterial blood, leading to increased levels of
CO2. Asthma causes bronchoconstriction, which restricts gas exchange and causes haemoglobin to
lose its affinity for oxygen. As a result. There is a reduction in the partial pressure of arterial oxygen
and the saturation level of SPO2. The chemoreceptor detects these low oxygen levels and activates
the respiratory centre in the medulla oblongata to compensate by increasing the respiratory
rate(Adrianne Dill Linton & Mary Ann Matteson, 2019) . In addition, inflammatory changes and
mucous production limit the patients' elastic recoil, necessitating the use of accessory muscles such
as shoulder muscles for breathing. Inflammatory mediators cause air trapping, resulting in impaired
expiration and decreased air trapping. This leads to hyperinflated lungs, V/Q mismatch, hypoxemia,
and hypercapnia, as well as shortness of breath and physiological changes. Peter’s blood gas analysis
reveals commonly observed elevated carbon dioxide levels and decreased oxygen levels, which can
be attributed to inadequate ventilation caused by air flow limitation. This limitation results in
impaired gas exchange and respiratory acidosis (Hales, 2019).