Pathophysiology of Asthma

Pathophysiology ofAsthma

Asthma refers to a common but chronic inflammatory airways disease.It is characterized by a number of variables with recurring symptoms,bronchospasm, and reversible airflows obstructions. Some of itscommon symptoms are wheezing, infrequent breathing, chest tightness,and coughing. There are a number of factors, including genetic andenvironmental, that are thought to cause Asthma. To diagnose is oftenbased on specific patterns of the recurring symptoms, spirometry, andhow it respond to therapy (McPhee, 2003). The paper aims atdescribing pathophysiological mechanisms of both chronic and acuteexacerbation of asthma, and the patterns created by the arterialblood gas during the exacerbation. Additionally, how environmentalfactor will impact be on Asthma’s pathophysiology. Again, two mindmaps will be created with the description of how diagnosis andprescription is done based on the selected factor.

Asthmaexacerbations are known to an exaggerated response from the lowerairway when exposed to the environment. Pathophysiological mechanismsof both chronic and acute asthma are divided into three components:Airway inflammation, bronchial hyper responsiveness, and intermittentairflow obstruction. First, airway inflammation may be acute orchronic (Huether &amp McCance, 2008). The presence of mucussecretions and airway edema contributes to obstruction of airflow andbronchial reactivity. Identified principal cells include macrophages,eosinophils, mast cells, and epithelial cells. Airwayhyper-responsiveness or hyper-reactivity bronchial presence refers toexaggerated response to a number of stimuli e.g. endogenous andexogenous. Chronic airway inflammation is thus associated with risein bronchial hyper-responsiveness (Huether &amp McCance, 2008). Thisleads to typical symptoms and bronchospasms, which leads to wheezing,coughing, and difficulty in breathing.

Airflowobstruction is triggered by a number of changes, which include acutebronchoconstriction, airway remodeling, plug formation of chronicmucous, and airway edema. Airway obstruction triggers increasedairflow resistance and decrease in the rates of expiratory flow. Suchchanges result in decreased ability to carry out expulsion of air,and could lead to hyperinflation. This could also alter pulmonarymechanics and rise in the rate of breathing. With Bronchialhyper-responsiveness, it compensates for airflow obstruction.However, compensation is often limited when tidal volume nearspulmonary dead space volume, and it result in alveolarhypoventilation (McPhee, 2003). Increased ventilation and worseningobstruction, early stage of acute episode of Asthma, as a result ofhyperventilation.

During an exacerbation, there are certain pattern changes that takeplace in the arterial blood gas. Asthma exacerbations includeepisodes of progressed worsening difficulty in breathing, wheezing,coughing, and chest tightening. All this are a result of change inpattern of arterial blood gas. Changes are seen based on the changesin PaO2. At start of Asthma attack, PaO2 of 100 mm Hg falls to 40 mmHg, and thus the disease worsens. When it reaches a point where thelungs fail to remove more carbon dioxide, Pa02 begin to rise and PHfalls (McPhee, 2003). When the attack worsens, PaO2 and the PHreverse to the normal rates.

Environmental factor is associated with the development of Asthma andits exacerbation. This environmental factor is broken down to includeair pollution, allergens, and environmental chemicals. These factorsare known to affected pathophysiology of both exacerbations ofAsthma. Chemicals from smoking for example, are often associated withthe symptoms of Asthma. Instances of high pollution rates fromfactors such as traffic or ozone, result in low quality of air arealso known to impact on the early development of acute Asthma andcontinuous increase in the condition’s severity (Huether &ampMcCance, 2008). Volatile gases also trigger mild Asthma, for example,exposure to formaldehyde. What these examples of environmental gasesdo is that they do not support causal roles. Rather, these factorsare able to tract infection, which compels development ofepidemiological evidences by lining it to the condition. Theseenvironmental factors create a barrier between the person andinhalation of good quality air. Pathophysiology of both disorders isthus worsened by the low quality, which is also an intricateinvolvement with allergic factors of the disorders.

To diagnose a patient with Asthma based on the environmental factorselected, I would first ask questions to come up with its nature andseverity of the symptoms. I will ask questions on the type ofenvironmental factors the patient has been exposed to. I will performphysical examinations with more focus on the skin, chest, and tractof the patient (Glissman, 2012). I will also examine thehyper-expansion of the shoulders, thorax, and deformity on the chest.Any signs of difficulty in breathing, wheezing sound, and fight forair through prolonged inhalation could suggest Asthma. Additionally,since environmental factors involve air, I would use a spirometer totest the patient’s lungs, to determine air obstructions. Treatmentof Asthma is achieved through periodic self-assessment of daily diaryof medications. Prescription of medications is often done followed byprovision of corticosteroid (Briscoe, 2012). Again, the patient isoffered oxygen therapy, especially when the disease is caused byenvironmental allergens. The allergens, however, should first beidentified. Such allergens are eliminated through embracing balanceddiet and avoiding alcohol and tobacco.

Chronic Asthma Exacerbation


Incidence rate measures disease onset and give information about the chances of the disease developing. Prevalence seeks to estimate the disease presence within a population. Mortality and Morbidity compares both rates of the disease prevalence around the world.


Bronchoconstriction, Airway hyper-responsiveness, Airway edema, and Airway remodeling.

Clinical Presentation

It involves its history on a family’s Asthma, sinusitis, allergy, and the nasal polyps. It helps to determine the rapidity of the onset, symptoms, and associated illnesses.


Evidence of permanent alterations, often in the path of airway structure (airway remodeling).


Controller medications and quick-relief medications e.g. Leukotriene modifiers, beta-agnostics, mast cell stabilizers. Corticosteroid

Acute Asthma Exacerbation


Acute episodes of progressive worsening of breathing difficulties, chest tightness, wheezing, or a combination of expiratory airflow decrease in lung function.


Airway edema, bronchoconstriction, and Airway remodeling.

Clinical Presentation

Clinical presentation examines findings of its likelihood, possible identification of its causal factors, and acute severity.


Physical examination on the skin, tract, and chest of the patient. Paying attention to breathing, prolonged inhalation, and presence of wheezing sound.


Well-balanced diet and anti-inflammatory drugs


Briscoe, K. (2012, May 12). Thetford: mother of Bradley Wilson,who died of asthma attack, told there was nothing she could havedone. East Anglian Daily Times. Retrieved from

Glissman, B. (2012, May 21). Girl`s death puts focus on asthma`sbroader grip. Omaha World-Herald. Retrieved from

Huether, S. E., &amp McCance, K. L. (2008). Understandingpathophysiology. St. Louis, Mo: Mosby/Elsevier

McPhee, S. J., Lingappa, V. R., &amp Ganong, W. F. (2003).Pathophysiology of disease: An introduction to clinical medicine.New York: Lange Medical Books/McGraw-Hill.