inflammation (Busse et.al. 1993). There is emerging evidence that stress can play a .
role in precipitating asthma exacerbations. The mechanisms involved have yet to be .
established and may include enhanced generation of proinflammatory cytokines .
(Friedman et. Al. 1994). Airway wall edema, even without smooth muscle .
contraction of bronchoconstriction, limits airflow in asthma. Increased microvascular .
permeability and leakage caused by released mediators also contribute to mucosal .
thickening and swelling of the airway. As a consequence, swelling of the airway wall .
causes the airway to become more rigid and interferes with airflow. Chronic mucus .
plug formation. In severe intractable asthma, airflow limitation is often persistent. In .
part this change may arise as a consequence of mucus secretion and the formation of .
inspissated mucus plugs. In some patients with asthma, airflow limitation may be.
only partially reversible. The etiology of this component is not as well studied as .
other features of asthma but may relate to structural changes in the airway matrix that.
may accompany longstanding and severe airway inflammation. There is evidence that .
a histological feature of asthma in some patients is an alteration in the amount and.
composition of the extracellular matrix in the airway wall. (Djukanovic et. El 1990; .
Laitinen and Laitinen 1994). .
Nursing goals for Lisa Lambos would be to maintain a good effective airway and.
relieve bronchoconstriction, while allowing mucus plug expulsion. This could be .
accomplished by assisting Lisa to sit in an optimal position, perform coughing and .
breathing manoeuvres. Lisa needs to be instructed to use a pillow or hand splints .
when coughing, to use abdominal muscles for more forceful cough, the use of an .
incentive spirometer and the importance of ambulation and frequent position changes .
directed coughing techniques help mobilise secretions from smaller airways to .