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Nursing Related Case Study
Tom's vitals, in the emergency department, revealed an elevated respiratory rate, heart rate and blood pressure. His oxygen saturation was also considerably low. Tom's Body Mass Index (BMI) falls in the overweight category. He was also a-febrile, at presentation, indicating that infection was not a precipitating cause.
Initially the ABGs were normal, indicating an acute severe exacerbation or life threatening asthma. Later, when the ABGs were repeated, carbon dioxide levels were above normal. A raised carbon dioxide level is the differentiating bench mark between life threatening and near fatal asthma. The ABG analysis also reveals acidemia which cannot be solely attributed to a respiratory or metabolic cause alone, and hence can be safely classified as a mixed disorder.
Tom's history is typical of atopic asthma which usually begins in childhood and is triggered by antigens from the environment, such as pollen, animal dander or dust. Upper respiratory tract infections and Aspirin can also trigger asthma. In such cases, patients with underlying atopy have a more sustained and severe attack. (Kumar & Robbins, 2007)
When an asthmatic patient comes in contact with an agent he is allergic to, the patient develops IgE antibodies. Mast cells then attach to these antibodies and, on further encounter with the allergen, these mast cells degranulate and release different inflammatory mediators such as leukotrienes, bradykinin and eosinophillic chemotactic factors. These factors in effect induce edema in the walls of small bronchioles, causing them to constrict. In addition, they also cause secretion of mucus into the lumen of the bronchioles and trigger spasm of the bronchial smooth muscles. The result is an increase in airway resistance. Asthma is, therefore, known as an obstructive airway disease, in which there is impairment of expiration. (Kumar & Robbins, 2007)
To understand the pathology behind the symptoms of asthma, it is first important to understand its mechanics. The normal muscles of inspiration are the diaphragm, external intercostals and the interchondral part of the internal intercostals. Normally expiration is passive since the lung-chest wall system is elastic and returns to its mean position after each inspiration and therefore, it does not require the use of muscles. In asthma, since there is airway resistance due to inflammation, patients use accessory muscles to overcome the resistance. This increases the work of breathing. The accessory muscles are the abdominal muscles and the internal intercostals muscles. The use of accessory muscles indicates respiratory distress. (Guyton & Hall, 2011)
On inspiration, in asthmatics, the inspiratory muscles contract and cause an increase in thoracic volume. This causes the alveolar pressure to decrease to below atmospheric pressure (thus making it negative). Negative intra-thoracic pressure allows air to flow into the lungs due to pressure gradients. Intra-pleural pressure also becomes more negative due to the elastic recoil capability of the lungs. There is an increase in overall lung volume. During expiration, normally alveolar pressure exceeds atmospheric pressure, reversing the pressure gradient allowing air to move out of the lungs. Intra-pleural pressure comes back to baseline, however, during a forceful expiration the intra-pleural pressure becomes positive causing the compression of airways and making it difficult to expire. (Guyton & Hall, 2011)
In asthma, the forced expiratory volume in the first second of forceful expiration, FEV1, is reduced. The forced vital capacity, FVC, which is the volume of air that is forcefully expired after inspiration, is also reduced. Normally the FEV1 to FVC ratio is 0.8, however in asthmatic patients; this value is reduced and can go as low as 0.2. The forced residual capacity (the lung volume after forced expiration) and residual volume increase in an acute asthmatic attack due to resistance to airflow. (Guyton & Hall, 2011)
Researches show a direct relationship between BMI and severity of asthma. Obesity has the capacity to impact lung functions in a variety of ways. These factors are poorly understood but are hypothesized to be due to the following reasons. Lungs of individuals who are overweight are under expanded and the size of breaths are shallower. This decreases the expansible properties of the lungs, making it more susceptible to the severity of asthma. In addition, obese individuals exhibit a chronic low grade inflammation, which can increase the frequency of asthma exacerbations. There are also changes in the blood levels of hormones derived from fat tissue, in individuals with a high BMI, which may affect the airways. Two of these hormones, leptin, which is pro-inflammatory, and adiponectin, which has anti-inflammatory properties, are disturbed in obese individuals. They have a tendency to accumulate increased amounts of leptin without counter-regulating its effects with adiponectin. (Myron, 2005) Tom has a BMI of 27.7, which indicates that he is overweight. This may be a factor contributing to his asthma severity.
V/Q is the ventilation perfusion ratio in the lungs. When the ventilation perfusion ratio is below normal, this indicates a physiologic shunt, which means that there is not enough ventilation which is required to fully oxygenate the blood flowing through the alveolar capillaries. When the ventilation perfusion ratio is above normal, this indicates physiologic dead space, which means there is enough ventilation but it goes to waste since there isn't adequate perfusion. In asthmatic patients, since there is obstruction of the airways, there is a V/Q mismatch. In some areas of alveolar units there is serious physiologic shunt, whereas in other areas, there is a physiologic dead space. This reduces the lungs capacity to function as an effective organ for gaseous exchange. (Guyton & Hall, 2011)
Acute, severe asthma can profoundly alter the cardiovascular status and function, as is the case with Mr. Tom. These are influenced by several factors, such as the duration and gravity of the disease, frequency of exacerbations, and severity of pathological changes in the broncho-pulmonary apparatus. Early and in mild forms of the disease, the circulation is hyperkinetic due to an increase in permeability of the vasculature, triggered by hypoxia. As the pathological changes in the lungs and myocardium increases, hypokinetic type of circulation develops. (Boon, Colledge, Walker & Hunter, 2010)
Tom's condition is progressing towards near fatal asthma. He has developed severe acidemia. At this stage, Tom may be expected to be suffering from severe hemodynamic compromise.
Hemodynamic changes in asthma can affect ventricular filling and the ejection fraction of the heart. In severe asthma, because of the effects of dynamic hyperinflation, the systemic venous return decreases significantly during expiration, and again rapidly increases in the next respiratory phase. Rapid right ventricular filling in inspiration shifts the inter-ventricular septum toward the left ventricle. This may lead to left ventricular diastolic dysfunction and incomplete filling. Systolic emptying is also impaired due to the large negative intra-thoracic pressure generated during inspiration. This increases the left ventricular afterload. Pulmonary artery pressure may also be increased due to lung hyperinflation and increased blood flow due to hypoxia, thereby also causing an increase in the right ventricular afterload. These events in acute, severe asthma may exacerbate the normal inspiratory reduction in left ventricular stroke volume and systolic pressure, leading to the appearance of pulsus paradoxus. (Boon et al., 2010)
A difference of more than 12 mmHg in systolic blood pressure between inspiration and expiration represents a sign of severity in asthmatic crisis. Eventually, the respiratory muscles fatigue and the difference in pressure between inspiration and expiration may decrease or disappear. Such status harbingers impeding respiratory arrest and arrhythmias. (Boon et al., 2010)
Asthma is characterized by airway hyper-responsiveness or bronchial hyper-reactivity. This exaggerated response is triggered through a cascade of adrenergic receptor stimulation, interleukins and other chemical mediators. The degree of airway hyper-responsiveness generally correlates with the clinical severity of asthma. (Kumar & Robbins, 2007)
There are two types of responses in asthma: acute and late response. The acute response is mediated directly through inhibition of beta 2- adrenergic receptors and activation of sub-epithelial vagal receptors. These receptors are present in a variety of cell types, for example, in smooth muscle and epithelial cells of the respiratory tract, in the endothelium and smooth muscle cells of vessel walls, and in inflammatory cells such as mast cells, eosinophils, and lymphocytes. (Kumar & Robbins, 2007)
Exaggerated vagal tone activation, due to excess acetylcholine release, causes an increased expression of downstream signaling components in airway smooth muscles, causing bronchoconstriction. Vagal stimulation also increases mucus production. Acetylcholine, acting through muscarinic receptors, may also be responsible for changes associated with airway modeling. This includes, basement membrane thickening, glandular and smooth muscle hypertrophy, and an increase in inflammatory infiltrates. (Kumar & Robbins, 2007)
On the other hand, effects of beta 2-adrenergic receptor activation in the lung include: smooth muscle relaxation, inhibition of acetylcholine release, increasing ciliary activity, decreasing mucous viscosity, increase in bronchial blood flow, reduction in vascular permeability, and inhibition of mediator release from some inflammatory cells. Beta 2-Adrenergic receptors are present in normal or increased numbers on asthmatic airway smooth muscle but are uncoupled in severe asthma. This hypo-responsiveness is due to the effects of inflammatory mediators. There is also evidence for dysfunction of beta 2-adrenergic…[continue]
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