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Acute Severe Asthma: Pathophysiology, Symptoms, and Nursing Strategies

   

Added on  2023-06-03

9 Pages2330 Words365 Views
Running head: ACUTE SEVERE ASTHMA
Concept Map and Guided Response
Name of the Student
Name of the University
Author Note

1
ACUTE SEVERE ASTHMA
Answer: 1
Asthma is a chronic lung disease which has no cure but can be effectively controlled
(National Asthma Council Australia, 2017). According to Christensen, Craft, Wirihana and
Gordon (2015), the main pathophysiology underlying asthma include inflammation in the
airway causing hyper-responsiveness and mucus hyper secretion which results in the
obstruction in the airflow. This obstruction in the airflow is the reason underlying the
dyspnoea as experienced by Jason Smith who was suffering from acute severe asthma. Other
symptoms of blockage in the airway occurring include cough, tightness in chest and wheeze.
These additional symptoms also coincide with the clinical manifestations of Jackson Smith at
the time of Emergency Department: diminished sound of breath and widespread wheeze. It is
due to tightness in chest that Jackson Smith was experiencing severe breathlessness along
with high respiratory rate (32 beats per minute with normal rate of 20 beats per minute).
Asthma is associated with other immunological processed like increase in the
concentration of CD4+ T lymphocytes along with increase in the secretion of the type 2 t
helper (Th) cells along with cytokine mediators like IL4, IL5 and IL13. All these cytokine
mediators are type hypersensitivity mediators, which causes inflammation and obstruction in
the airway (Graziottin & Serafini, 2016). The activation of the type 1 hypersensitivity
reactions leads to degranulation of the mast cells along with the release of the type 1
hypersensitivity mediators like histamine, interleukins, leukotriene, prostaglandins and nitric
oxide. All these type 1 hypersensitivity mediators have vasoactive effects, which causes
vasodilation along with increase in the capillary permeability. Increase in capillary
permeability increases the blood flow in the lings along with increase in the infiltration of the
inflammatory cells and chemotactic factors along with neutrophils, eosinophil and
lymphocytes. This increase in the flow of the blood is the reason underlying the increase in

2
ACUTE SEVERE ASTHMA
the blood pressure (150/85 mmHg) and pulse rate (130 beats per minute) for 18-year old
Jackson Smith (Graziottin & Serafini, 2016).
In addition to there is alteration of the normal autonomic control of the bronchial
smooth muscle cells due to the production of neuropeptides (small protein-like substances
which are released from the neurons in order to communicate with other neurons). The
release of the neuropeptides causes increase in the release of the neurotransmitter,
acetylcholine. The release of acetylcholine causes bronchospasm. Bronchospasm causes
long-term damage in the airway. It is due to bronchospasm that Jackson Smith is
experiencing laboured breathing or shortness in breath (Graziottin & Serafini, 2016).
Ostrom et al. (2013) highlighted that permanent damage cause by bronchospasm leads
to recurrent asthmatic attack as in case of Jackson who is suffering from asthma from a tender
age, 2 years. Increase in bronchospasm leads to bronchoconstriction. The increase in the
inflammatory mediators like IgE further increases the severity of bronchoconstriction and
leads to obstruction in the airways leads to wheezing sound of breath at the time of airflow.
Bronchoconstriction can also be defined as additional reason behind the increase in the chest
tightness of Jackson Smith. Ostrom et al. (2013) stated that wheezing is a type of musical
sound that is generated because of limited flow of the air into the lungs or the pulmonary
cavity.
The permanent change in the pulmonary airways caused through bronchoconstriction
is defined as airway remodelling. This leads to progressive loss of the smooth muscle
function in the lungs which is irreversible. Moreover, the oxygen saturation of Jackson Smith
was found to be marginally low, 90 SpO2 on room air (normal 95 to 98 SpO2). This low
oxygen saturation level leads to the generation asthmatic attack. Low level of oxygen
saturation is defined as a process of low amount of oxygen dissolved in blood. This low

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