The following essay will discuss the case of Mr Jones, who was admitted to the A&E department following a worsening of his symptoms of COPD. The focus of the essay is to provide a detailed plan of the management and emergency care of patients with exacerbations of COPD in A&E within the first two hours of their admission. The essay will guide us through Mr Jones’ stay at the A&E department with regards to the altered physiology of COPD and its acute episodes of exacerbations. Mr Jones’ worsened health condition and physical symptoms will be assessed in the light of his medical history. The author will also analyse the relevant literature and relate the clinical management not only to pathophysiology but also to the evidence base and clinical practice. The importance of providing patient-centered care will be emphasised in areas of consent and privacy and dignity of the patient. Responsibility and accountability in nursing profession will be underlined in the light of the NMC (2007) Code of Conduct for nurses and midwives. A summary of the main points of the discussed topic will be provided in the conclusion. All literature will be referenced with adherence to the Harvard Referencing System.
Pathophysiology of COPD in acute exacerbations
Exacerbations of COPD can be described as increased airway inflammation and oedema, leading to systemic inflammation causing even more airflow limitation and worsening of ventilation and perfusion (Aaron et al, 2001). It can also be characterised by increased oxygen consumption, altered hypoxic vasoconstriction, and systemic and pulmonary haemodynamic abnormalities (increased cardiac output and increased pulmonary artery pressure) (Bhowmik et al, 2000; Dentener et al, 2001). The three main factors that contribute to the narrowing of the airways are peribronchial fibrosis, build-up of scar tissue from damage to the airways and over-multiplication of the epithelial cells lining the airways. Loss of lung tissue elasticity occurs as a result of destruction of the structures supporting and feeding the alveoli: the small airways collapse during exhalation, impeding airflow, trapping air in the lungs and reducing lung capacity (Chung, 2005). Inflammation enlarge the mucous glands that line airway walls in the lungs, causing goblet cell metaplasia and leading to healthy cells being replaced by more mucus-secreting cells. As inflammation continues, the airways constrict, becoming excessively narrow and swollen. This leads to excess mucus production and poorly functioning cilia, a combination that makes airway clearance especially difficult, resulting in a chronic, productive cough, wheezing and dyspnea (Vermeeren et al, 1997). Stimuli that irritate the lungs attract and activate several cell types, including neutrophils, eosinophils, macrophages, monocytes and lymphocytes that contribute to pulmonary inflammation (Barbera et al, 1997). The build-up of mucus attracts a host of bacteria that multiply in the environment of the airway and lungs, contributing to excess mucus in the airways which eventually will accumulate and block them, leading to further worsening of the airflow (Danahay and Jackson, 2005). The end result is the formation of diverticula in the bronchial tree, and bacterial lung infection, a common cause of COPD exacerbations Alveolar hypoventilation and respiratory muscle fatigue contribute to hypoxaemia, hypercapnia and respiratory acidosis leading to severe respiratory failure and death (Stevenson et al, 2005). Aims of nursing care and management of exacerbations of COPD within the first two hours in A&E
Mr Jones presented to the A&E with the following symptoms: increased breathlessness, increased sputum purulence, increased wheeze and reduced exercise tolerance. Test results showing slight pyrexia (37.2); SpO2...