Acute Severe Asthma: Definition, Etiology, Pathogenesis, Signs and Symptoms

This article discusses Acute Severe Asthma, its definition, etiology, pathogenesis, signs and symptoms. It also explains the mode of action of drugs and nursing implications for their use.

RUNNING HEAD: Acute Severe Asthma 1
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Question 1
a) Definition and etiology
Asthma is characterized by airway hyper responsiveness to normal stimuli, reversible
airflow obstruction and variable airflow as show by Peak Expiratory Flow. Its pathogenesis
involves both environmental and genetic factors. The later includes atopy, a positive family
history of asthma and intolerance identified as polygenic. Gender and ethnicity also play a role at
different stages of life (Ferreira, et al., 2017). Perfumes, pollen, dust, smoke from industries and
car exhaust fumes have been identified as environmental factors that play a role in asthma
progression. Dietary deficiency of vitamins C and E (antioxidants) have been shown to
predispose to asthma. Pollution from indoors like dust, pets and pests are also triggers for
asthma. (Maslan & Mims, 2014). Oral contraceptives and non-steroidal anti-inflammatory drugs
like aspirin and diclofenac, when used for long can lead to one developing asthma. It is possible
that Smith’s problem can be traced from the family, and accentuated by environmental factors.
(Kumar, Abbas, & Aster, 2015). Environmental and genetic factors, when combined, produce an
additive effect for asthma progression. The hall mark of the asthma is airway inflammation,
edema of mucosa, bronchoconstriction, hypertrophy of smooth muscles of the bronchus and
mucous gland (Lambrecht & Hammad, 2015)
b) pathogenesis
Genetic susceptibility to asthma, an example of type 1 hypersensitivity reaction (atopy)
plays an important role in development of asthma. Upon exposure to an offending agent,
inflammation ensues (Craft et al, 2015.)Eosinophils and neutrophils are the major inflammatory
cells recruited. In atopic asthma, TH2 production is too much. It fuels production of IL-4 which in

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turn stimulates production of IgE (produced by B cells). B cells are activated by IL-13 which
also stimulates mucous production (Craft et al, 2015). IL-5 activates eosinophils. Degranulation
happens when IgE coats mast cells, making the membrane become unstable and release
inflammatory cytokines, initiating early and late responses of asthma. Increased mucus
production, vasodilation and bronchoconstriction mediated by vagal stimulation in the
epithelium is characteristic of an early wave (Lambrecht & Hammad, 2015). Eosinophils,
neutrophils and T cells are activated in the late phase. Continuous chemotaxis and activation of
TH2 cells amplify the reaction. (Kumar, Abbas & Aster, 2013). Repeated exposure to allergen
causes airway remodeling that has hypertrophied muscles and mucous glands that makes the
airway narrow (Craft et al, 2015).
Signs and symptoms
Jackson Smith presents with Acute Severe Asthma (ASA) that is usually unresponsive to
corticosteroid and bronchodilator therapy. Severe dyspnea is due to airway hyperactivity to an
allergen causing inflammation and increased mucus production that limit amount of air entry and
outflow (Kumar, Abbas & Aster, 2013).Airway remodeling is also a causative factor. Narrowing
of lumen causes increased respiratory effort to deliver more oxygen and wash out carbon dioxide
Respiratory center is sensitized by excess carbon dioxide (as Jackson Smith’s) to wash out
excess CO2. Oxygen saturation at room air was low in Smith’s case because of inadequate
oxygen delivery to blood by narrowed lumen of bronchi.
The body’s response for low oxygen tension in tissues is through increasing the blood
pressure and heart rate so that more blood with oxygen can be delivered per unit time. Asthma
attack leaves a patient with inadequate oxygen in tissues, causing blood to be redirected to other
vital organs like brain and heart (Craft et al, 2015). Smith’s blood pressure and pulse rate were

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increased so that more oxygen can be delivered in tissues per unit time, as part of physiological
body response. Physical examination, including auscultation revealed widespread wheeze and
reduced air entry in lungs. Narrowing of bronchi is responsible for reduced air entry and exit thus
the finding on auscultation. Wheeze is explained by air turbulence as it rushes in the narrowed
lumen of the bronchi. Hyperinflation of lung fields on chest X-ray is due to chronic air trapping
in lungs (Pijnenburg, et al., 2015).
Blood gas analysis performed on Smith shows abnormal values. There is renal
compensation of respiratory acidosis as shown by high PaCO2 of 50 mmHg (Normal is 35-45
mmHg) (Pijnenburg, et al., 2015). This is evident of long time respiratory distress. Asthma
makes the patient inhale inadequate oxygen and makes exhalation of carbon dioxide incomplete
therefore accumulating excess carbon dioxide. When excess carbon dioxide dissolves in blood,
weak carbonic acid is formed, hall mark for respiratory acidosis. Weak carbonic acid further
degrades to hydrogen ions as shown by Magge, Pascanu & Salerno, (2017). Excess hydrogen
ions is buffered by bicarbonate ions. The kidneys increases absorption of bicarbonate ions to
buffer the low pH. Patients hyperventilate in acute states of respiratory distress, a process leading
to respiratory compensation of respiratory acidosis as shown by National Asthma Council
Australia, (2017).
Question 2:
Two high priority interventions that should be undertaken by nurses to manage Smith’s
ASA are bronchodilator therapy initiation and oxygen administration. Severity of the attack can
also be assessed as described in by the National Asthma Council Australia, (2017).

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Salbutamol, 12 puffs equivalent to 100 mcg per actuation using pressurized metered dose
inhaler (pMDI) and a spacer is the desired bronchodilator therapy (National Asthma Council
Australia, 2017). 5mg of salbutamol in a nebulizer is used in cases where the patient cannot
breathe. Oxygen, via a high pressure flow (venturi) system should be given targeting a saturation
of above 94% in young patients like Smith (National Asthma Council Australia, 2017).
Assessing patient’s condition while giving bronchodilator and oxygen therapy is
necessary. Repeat doses of salbutamol (3 doses in 1 hour) or in PRN form should be initiated.
Ipratropium bromide, 8 puffs through pMDI or 500 mcg nebule added to salbutamol is added in
cases of poor response. 37.5-50 mg oral prednisolone, a systemic corticosteroid (for 5 days) or
100 mg of intravenous hydrocortisone every 6 hours is also given to slow down inflammation
(National Asthma Council Australia, 2017). Therapy response is reviewed after a week and
recorded (National Asthma Council Australia, 2017). A step down therapy started if a good
control has been achieved. Calculation of Smith’s minimum dose of drug is also done and during
this period, symptoms and peak expiratory flow rate is monitored then a follow up visit
scheduled (Aitken, Marshall, & Chaboyer, 2015). Drug shelf life is also checked to make sure it
is still viable.
Question 3
a) Mode of action of drugs
Ipratropium is a short acting anti muscarinic drug that has competitive binding properties
to cholinergic receptors of bronchial smooth muscles. It blocks acetylcholine therefore inhibiting
bronchoconstriction. Vasodilation and bronchodilation is the ultimate effect of inhibition of
vagal stimulation in sub epithelium (FitzGerald et al., 2018).

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Salbutamol acts via the G-protein coupled pathway. It is a short acting beta 2 agonist.
cAMP and protein kinase A is activated upon stimulation of G protein (Carotenuto, Perfetti,
Calcagno, & Meriggi, 2018). There is activation of myosin light chain phosphatase that enables
entry of calcium via gated ion channels causing smooth muscle relaxation. This causes
bronchodilation.
Intravenous hydrocortisone is a systemic corticosteroid (Radojicic, Keenan, & Stewart,
2016). It works by inhibiting inflammatory path in asthma by blocking phospholipase A2 that
supressesLipocortin-1. Phospholipase A2, when blocked will lead to depletion of eicosanoids.
Therefore inflammatory cells recruitment is suppressed (Kumar, Abbas & Aster, 2013).
a) Nursing implications for the use of drugs
Monitoring for therapeutic effects of ipratropium bromide, hydrocortisone and
salbutamol is one of the nursing implications (Johnson, 2017). Patient improvement and side
effects should also be monitored. For instance, low potassium levels and tachycardia after
salbutamol use (especially in overdose) , dry mucous membrane, urinary retention and slow heart
rate for ipratropium bromide and glucose intolerance, infections susceptibility and weight gain
in prolonged use of hydrocortisone should be looked into. Liver and renal function tests should
be monitored. Correct route, dosage and shelf life of the drug should also be looked into when
the patient is not responding to therapy (Ojo et al., 2014).

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References
Aitken, L., Marshall, A. & Chaboyer, W. (2015). ACCCN’s critical care nursing (3rd ed.).
Chatswood, NSW: Elsevier Australia. Chapter 10.
Craft, J.A., Gordon, C.J., Huether, S.E., McCance, K.L., Brashers, V.L. & Rote, N.E. (2015).
Understanding pathophysiology – ANZ adaptation (2nd ed.). Chatswood, NSW: Elsevier
Australia. Chapter 24 & 25.
Ferreira, M. A., Jansen, R., Willemsen, G., Penninx, B., Bain, L. M., Vicente, C. T., & Baltic, S.
(2017). Gene-based analysis of regulatory variants identifies 4 putative novel asthma risk
genes related to nucleotide synthesis and signaling. Journal of Allergy and Clinical
Immunology, 139(4), 1148-1157.
Johnson, R. A. (2017). A Quick Reference on Respiratory Acidosis. Veterinary Clinics: Small
Animal Practice, 47(2), 185-189.
Kumar, V., Abbas, A., & Aster, J. (2013). Robbins Basic Pathology (9th ed., pp. 468-470).
Canada: Elsevier Saunders.
Lambrecht, B. N., & Hammad, H. (2015). The immunology of asthma. Nature immunology,
16(1), 45.
Magge, A., Pascanu, R., & Salerno, E. (2017). C58 CRITICAL CARE CASE REPORTS:
NOTABLE CAUSES AND COMPLICATIONS IN ACUTE RESPIRATORY
FAILURE: Extracorporeal Membrane Oxygenation in Patients with Acute Severe
Asthma. American Journal of Respiratory and Critical Care Medicine, 195.

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Maslan, J., & Mims, J. W. (2014). What is asthma? Pathophysiology, demographics, and health
care costs. Otolaryngologic Clinics of North America, 47(1), 13-22.
National Asthma Council Australia. (2017) Australian Asthma Handbook – Quick Reference
Guide, Version 1.3. National Asthma Council Australia, Melbourne. Available from:
http://www.asthmahandbook.org.au
Ojo, O. O., Basu, S., Jha, A., Ryu, M., Schwartz, J., Doeing, D., ... & Halayko, A. J. (2014). D29
MOLECULAR SIGNALS AND CELLULAR MECHANICS: FOCUS ON ASTHMA:
S100a8/a9 Is A Mediator Of Asthma Pathophysiology In An Acute Allergic Model Of
Asthma. American Journal of Respiratory and Critical Care Medicine, 189, 1.
Pijnenburg, M. W., Baraldi, E., Brand, P. L., Carlsen, K. H., Eber, E., Frischer, T., ... &
Mantzouranis, E. (2015). Monitoring asthma in children. European respiratory journal,
45(4), 906-925.
Radojicic, D., Keenan, C. R., & Stewart, A. G. (2016). The Physiological Glucocorticoid (GC),
Hydrocortisone, Limits Selected Actions Of Synthetic GC In Human Airway Epithelium.
In A40. EPITHELIAL REGULATION OF INFLAMMATION (pp. A1472-A1472).
American Thoracic Society.

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