leads to other adaptive immune responses [ CITATION Bra19 \l 1033 ]. The pathophysiology of
these alterations result in the symptoms of having an obstructed airway such as coughing,
wheezing, labored breathing, chest tightness, ands shortness of breath [ CITATION Bra19 \l 1033
].
The second stage of cellular response is called the late asthmatic response phase.
During
this phase leukotrienes, eosinophils, and toxic neuropeptides are released. This causes further
bronchospasm, edema, and increased mucus secretion resulting in airway obstruction
[ CITATION Bra19 \l 1033 ].
Airway obstruction causes impaired airflow and uneven
ventilation in the lungs. Some areas hyperventilate because of air trapping .It also causes
increased resistance and decreases expiratory flow [ CITATION Bra19 \l 1033 ]. This increased
air trapping can cause decreased perfusion to the alveoli.
Alteration in gas exchange make it
difficult for the lungs to effectively expel CO2.
This causes the body to compensate for this
early hypoxemia through hyperventilation.
If the asthmatic response is not stopped at this point,
the hyperventilation will lead to respiratory acidosis [ CITATION Bra19 \l 1033 ]. Respiratory
PATHOPHARMACOLOGICAL FOUNDATIONS
4
acidosis can be fatal because it causes the PaCO2 to rise. The human body is unable to
compensate for a PaCO2 over 70mmHg. An additional sign of impending death is also noted
when an asthmatic has no audible air movement [ CITATION Bra19 \l 1033 ].
Standard of Practice
The standards of practice in my facility differ from an emergent case to chronic care. We
will focus on chronic care in this section due to the numerous phenotypes of asthma. The
standard practice begins with diagnosing the patient with asthma. This is done with the
administration of lung function tests. These tests include a peak flow meter and spirometry
testing. Additional tests that can assist in the asthma diagnosis are: allergy testing, imaging,
methacholine inhalation challenge, nitric oxide test, sputum eosinophils and stress tests
[ CITATION AMI191 \l 1033 ]. After a patient has been diagnosed with asthma the standards are
to determine the phenotype. For example is it allergic asthma, exercised induced asthma or age-
on-set asthma [ CITATION Bra19 \l 1033 ]. Providers treat asthma with trigger avoidance,
patient self-monitoring, medications and if necessary Bronchial Thermoplasty which is an
outpatient procedure for the treatment of severe asthma in adult patients [ CITATION AMI191 \l
1033 ].
Medications for daily treatment can include inhalers, intravenous medications and oral
medications. Treatments will differ on whether the asthma is well controlled, partially controlled
or not controlled. The use of a daily medication that controls the symptoms and reduces the
inflammation and the risk for an acute exacerbation is the first step. These medications would
include a low-dose inhaled corticosteroid (ICS) [ CITATION RTS \l 1033 ]. The next step would
be the daily medication used in combination with an as needed reliever. These medications
PATHOPHARMACOLOGICAL FOUNDATIONS
5
include a short-acting beta-2-agonist (SABA) to reduce the symptoms of an acute asthma
exacerbation [ CITATION RTS \l 1033 ]. Additional therapy is considered when severe asthma
