Asthma is a chronic airway disease typified by airway inflammation and intermittent airflow obstruction producing symptoms of cough, wheezing, and chest tightness (Corren et al. 2011). Inflammatory and structural changes throughout the airway result in bronchial thickening and edema, bronchoconstriction and increased production of mucus, which together contribute to the episodic obstruction in airflow characteristically found in asthma (Doeing&Solway 2013). Acute pulmonary edema is condition caused by fluid accumulation in the lungs. The resultant fluid congestion decreases gas exchange across the alveoli leading to decrease blood oxygenation, and sometimes, carbon dioxide accumulation (Her 2010). Asthma and acute pulmonary edema may be linked pathophysiologically. The severe bronchospasm that occurs in patients with asthma results in the generation of a large negative intrathoracic pressure during spontaneous breathing (Krodel et al. 2011). The large negative intrathoracic pressure increases venous return in the right ventricle resulting in increased pulmonary blood volume. Intrathoracic negative pressure surrounding the descending thoracic parts of the aorta and the left ventricle holds thoracic blood volume resulting in increased left ventricular afterload (Her 2010). The increased left ventricular afterload and pulmonary blood volume increase hydrostatic pressure in the pulmonary capillary. Additionally, the negative intrathoracic pressure causes a decrease in pulmonary interstitial pressure (Rasheed et al. 2014). These factors ultimately lead to increased pressure gradient that favors filtration of edema fluid into the lung resulting in pulmonary edema (Her 2010). Acute pulmonary edema can also cause cardiac asthma. Patients with asthma and pulmonary edema are likely to present with cough, breathlessness, and production of sputum (Buckner 2013). Part 2 The existence of asthma and acute pulmonary edema as comorbidity can affect the diagnosis. The signs and symptoms of acute pulmonary edema can be very difficult to differentiate from those of asthma as both can cause breathlessness, cough and sputum production. This may, therefore, result in diagnosis overshadowing of either of these conditions (Bhaskar& Fraser 2011). Comprehensive history taking and physical examination is required to differentiate them. The existence of both conditions in the same patient is also likely to influence care priority because of the increased risk of respiratory failure (Bhaskar& Fraser 2011). Such patients, therefore, require priority emergency interventions to minimize adverse effects (Dunn et al. 2007). Both asthma and acute pulmonary edema are likely to negatively affect patient outcomes due to increased risk of mortality and morbidity. The comorbidity effect is that of worsened breathlessness, which increases the patient’s risk of respiratory failure and mortality. In addition, the comorbidities can cause pulmonary ischemia, which is also associated with poor patient outcomes (Her 2010). Part 3 Various factors are likely to influence transport and priority to tertiary care. The first factor is the severity of the asthma or acute pulmonary edema. A patient severe asthma or acute pulmonary edema that life threatening due to respiratory failure should be given priority for transport and transfer to tertiary care because delays in the initiation of life saving interventions can result in adverse patient outcomes (Her 2010). Second factor is age of the patient. Very young children or older adults should be given priority because they are at greater risk of adverse outcomes due to immature respiratory function and age-related decline in respiratory function respectively. Patients who have had these comorbidities for longer duration are likely to have progressive decline in lung function, and are, therefore, at greater risk of complications. Having these conditions chronically is also likely to affect other vital body organs such as the heart and the kidneys, impairing their functions. Such patients should be prioritized for tertiary care (Dunn et al. 2007).
