Acute Severe Asthma: Symptoms, Causes, and Management

Acute severe asthma triggers viral infection to the respiratory system, making the body to respond as in Jackson Smith case. The trigger could be an allergen, drugs cold air and others. Jackson Smith symptoms included severe dyspnea, low blood pressure, low pulse rate and auscultation of the lungs. Dyspnea is having difficulty in breathing, commonly in response to allergens exposure.

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Acute Severe Asthma:
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Guided answers questions
Acute severe asthma triggers viral infection to the respiratory system, making the body to
respond as in Jackson Smith case. The trigger could be an allergen, drugs cold air and others.
Jackson Smith symptoms included severe dyspnea, low blood pressure, low pulse rate and
auscultation of the lungs. Dyspnea is having difficulty in breathing, commonly in response to
allergens exposure. This could have been due to thickening of the airway passage walls and their
structural changes (airway remodeling) leading to bronchoconstriction. The airway obstruction
disrupts ventilation reducing oxygen intake and leads to ventilation-perfusion mismatch which
results to in the cut breathes 32 breathes per minutes and increased pulse rate to 130 beats/
minute to compensate the oxygen deficiency. The amplified pulse rate was a response by
Jackson’s body to neutralize the oxygen deficit.
Jackson's inability to inability to speak sentences in one breath was due to intrapulmonary
mechanism due to profound perfusion and ventilation mismatch. The low blood pressure 150/85
mmHg was due to the negative intrapleural pressure and hyperinflation in the lungs. The blood
pressure changes could be as a result of lymphocytes. The eosinophil responds to an increase in
response to exposure to an allergen this leads to inflammation of the airways hence affecting the
nasal passages and lower airways suppressing the breathing cytokines also modulate the airway
inflammation IL 13 inducing hyperresponsiveness of the IgE.
Results of the chest x-ray indicated that the lungs were inflated. This could have led to the
breathing difficulties and an attributing factor to the metabolic acidosis condition diagnosed after
arterial blood tests. ABG was to assess the extent of alveolar ventilation. Alveolar ventilation
decreases due to increased muscle fatigue and bronchospasm in response to dyspnea. The levels

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of carbon dioxide accumulation also increase (Griffin et al.,1992). Also, using the accessory
muscles during respiration increases oxygen consumption and production of carbon dioxide
leading to lactic acidosis and an acid-base imbalance. Metabolic acidosis could be due to the
development of ketones after strenuous muscle activity and dehydration due to increased
secretions. It could be attributed to hypoxia, increased work of breathing and lactate
accumulation.
Auscultation of lungs identifies diminished breath sounds and widespread wheeze caused
by airway remodeling as a result of activation of type 2 inflammatory cells that migrate to the
airway epithelium and subepithelial mucosa releasing IL 5 and IL 3(McFadden2003). The
smooth muscle hypertrophy and metaplasia goblet cell subepithelial fibrosis combine to narrow
the airway at the baseline altering its structural elements. The breathing difficulties due to
hyperinflation of the lungs since obstructed airways cause premature closure of the airway
leading to air being trapped hypoxemia occurs due to inhomogeneous distribution of oxygen to
the affected areas leading to ventilation/perfusion mismatch.
Based on Jackson smiths’ history of the asthmatic attack at 2 its reoccurrence at 18, could
be as a result of airway parenchyma uncoupling. This usually occurs with marked inflammation
that makes those who are genetically susceptible to get the attacks. Activated mast cells and
lymphocytes produce pro-inflammatory cytokines (PAF, PGd2 which increase the airways
bloodstream. There are also predisposing environmental factors that could have to lead this such
as availability of the allergen triggers exposure to an allergen, gastroesophageal reflux smoking,
sudden withdrawal from corticosteroids, cold air, exercise consumption of food or drugs such as
beta blockers.

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PaO2: 60mmHg (hypoxemia- decrease in oxygen): PaCO2 50mmHg (hypocapnia -
increase in carbon dioxide) indicates respiratory failure this could have been as a result of
frequent coughing to clear airway secretions.
Question 2
Management of Jackson’s critical condition aims at clearing the airway and improving
the respiratory system due to the shortness of breath. The first management strategy aimed at
offering relief of airway obstruction. Correction of marked hypoxia was important and reversal
of the airway blockages. Supplemental oxygen could be given to achieve 90% or more oxygen
saturation (Carroll &Schramm,2006). This is meant to promote bronchodilation and reduce
pulmonary constriction. Closely monitoring Jackson’s condition during this procedure is
essential to minimize the risk of oxygen toxicity. Repetitive administration of beta 2 agonists
bronchodilators through inhalation. This beta 2 agonists stimulate the beta 2 receptors on the
airway smooth muscles leading to relief in bronchoconstriction, which results in decreased
resistance inflow of air (Bone,1996). Short-acting beta 2 agonists (SABAs) be given since they
are known to offer quick-relief medications used in the treatment of bronchoconstriction.
Therefore, they are the best for the treatment of Jackson’s critical condition.
Nebulised salbutamol can be given intermittently on iv, since inhaled aerosolized routes may
not reach the lower airways and lung tissues due to severe obstruction of the airway and a
decrease in tidal volume
use of beta-agonists and corticosteroids because they are the pillars of initial treatment.
The second management strategy involves the maintain a clear area atmosphere and therapy
decisions to included to avoid recurrence. Administering Jackson with ipratropium bromide to

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early beta agonists treatments may reduce airway obstruction. Intravenous magnesium sulfate
may be employed as well. Inhaled corticosteroids are considered for most patients since they are
known to minimize lapses and to improve the patient's health this could improve Jackson’s
respiratory system hence reducing chances of the condition recurrence. Linking the discharge
plan to closely following up on Jackson’s case .the two management strategies mentioned above
will profoundly help in stabling Jackson’s case and reducing future recurrences as well.
Question 3
a)
The drugs given to Jackson Smith will help in stabilizing his acute severe asthma
condition. Nebulized salbutamol is given using t a face mask in the treatment of severe acute
asthma. It relaxes the smooth muscles of the airways by activating the beta 2 adrenergic receptors
in the lungs leading to activation of adenyl cyclase that leads to increased concentration of
cAMP which increases levels of AMP hence inhibiting the release of mediators from mast cell
which cause bronchospasm leading to bronchodilation.once the pathways dilate the difficulties in
breathing and the speechlessness
Administration of nebulized Ipratropium bromide which is an anticholinergic
parasympatholytic agent that blocks the muscarinic receptors of acetylcholine on the airways and
the nasal passages. Acetylcholine is used by nerves during communication with the muscles and
appears to inhibit vagally mediated reflexes by antagonizing the action of acetylcholine (Griffin
et.al,1992). A transmitter agent released from the vagus nerve block acetylcholine inhibits
cholinergic nerves leading to muscle relaxation and dilation of airways. Once the muscles are
relaxed Jackson’s shortness of breath will be resolved

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Administration of Intravenous hydrocortisone which is a corticosteroid aims at reducing
mucus secretion. This is achieved by inhibition of the release of secretagogue from macrophages.
They also inhibit the late phase reaction, by inhibiting the inflammatory response and interfering
with chemotaxis reactions in the body. This action results in the inhibition of LTB4 released due
to the eosinophilia effect. They also enhance beta-adrenergic response leading to relieve in
muscle spasm
b)
A nurse aids by assessing his response when therapy needs to be adjusted to improve patient
response and minimize adverse reactions. Evaluating and supporting the airway breathing
circulation. Jackson's vital signs (the blood pressure and pulse rates) to be check and recorded.
His clinical status assessed so that improvements or deteriorations can be made. Helping him
assume a comfortable position. Encouraging him on the importance of relaxing to reduce oxygen
consumption hence improving his condition. Ensuring the environment of the room and outside
is calm. Continually reassure Jackson that he is safe.
Monitoring the fluid balance and administering fluid replacement when he is dehydrated
because of increased oral intake and increased fluid loss caused by agitation. Maintaining
adequate intravascular volume is essential since mechanically ventilated patients are at high risk
of hypotension. Teaching the patient and his family about asthma control and prevention also
arrange follow-up management and enroll in programming aiming at explaining self-treatment.
Correction of marked hypoxia is important and carried out to reverse the obstruction.
Supplemental oxygen is given to achieve 90% or more oxygen saturation this will reversely

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promote bronchodilation and reduce pulmonary construction strictly monitor the patient during
this procedure to minimize the risk of oxygen toxicity.
administration of beta two agonists bronchodilators through inhalation .the beta 2 agonists
stimulate the beta two receptors on the airway smooth muscles leading to relief in
bronchoconstriction which leads to decreased resistance inflow of air. Short-acting beta 2
agonists (SABAs) are the quick-relief medications used in the treatment of bronchoconstriction.
Therefore, they are the best for the treatment of severe acute asthma. Nebulized salbutamol can
be given intermittently on iv since inhaled or aerosolized routes may not reach the lower
airways and lung tissues due to severe obstruction of the airway and a decrease in tidal volume

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References
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