Paper Example on Pathophysiology of Acute Respiratory Distress Syndrome

Introduction

The Acute Respiratory Distress Syndrome is a disorder that is associated with alveolar damage. According to Sarkar, Niranjan, and Banyal (2017), "it is the sudden injury to the alveolocapillary membrane, and it produces pulmonary inflammation, increased capillary permeability, severe edema, shunting, VQ mismatch, and hypoxemia." The Diffuse Alveolar Damage abbreviated to as the DAD and the Lung Capillary Endothelial injury are the most affected parts. The pathophysiologic process of this disease is divided into three stages. The stages are exudative, proliferative, and the fibrotic one. The pathophysiologic process of the ARDS can be explained concerning each scene.

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Exudative Stage

The exudative befalls happen within three days. Within this period, the affected person appears healthy as the symptoms do not manifest at this time. During this time, the injuries at the lungs trigger the neutrophils and other cells to cause more harm. McCance and Huether assert that "Activated complement factors and platelet aggregation result in the intravascular microthrombus formation and further damage to lung capillaries (2014)". The process is aggravated by the action of the neutrophils which discharges toxic mediators that run into the body to later damage the alveolocapillary. When this is destroyed, it makes the capillary more permeable thus allowing the passage or the leakage of fluids, blood cells, and food nutrients such as proteins (McCance & Huether, 2014).

Furthermore, continued permeability leads to pulmonary edema as well as hemorrhage which make the lungs not to perform as required. In addition, the alveoli ventilation is also hindered. Besides, the neutrophils are also responsible for discharging mediators that lead to vasoconstriction. As a consequence, blood flow to the lungs is decreased. It is at this stage where the respiratory bronchioles are filled with the fluid causing them to fail. As a result, a person develops breathing problems.

Proliferative

The stage's symptoms start appearing after one to three weeks. In this case, the pulmonary edema becomes intense where pneumocytes are produced with fibroblasts, and myofibroblasts are discharged. After a short while, the spaces in the alveolar are affected which translate to difficulties in respiration (Sharp, Millar& Medford, 2015). Such is depicted when patients have impaired breathing.

Fibrotic Stage

The stage becomes evident a fortnight after the lung injury. It is at this phase when the tissues at the alveoli, bronchioles, and interstitium wear out which later lead to the mismatch of the V/Q (McCance & Huether, 2014). Fluid around the lungs fills up the airspaces which cause the collapse of the alveolar. Due to this, respiratory failure sets in owing to systematic inflammatory. After the duration of time, the ARDS develops fully which leads to death.

Therefore, from our scenario, it is evident that the x-ray showed that the ARDS had progressed affecting the alveoli. Besides, it is worthwhile to conclude that the pulmonary edema and the alveoli had been filled up with fluids. It thus becomes the main reason for her to be ventilated in a hospital to check her against the lung destruction. Early detection is necessary in this case to ensure that the ARDS is detected earlier and treated before it worsens.

The Direction of Shift of Oxyhemoglobin Dissociation Curve

In the initial stages of the ARDS, the oxyhemoglobin dissociation curve would shift rightward. It is swung to the right side since the patient is suffering from respiratory problems. During hyperventilation, the patient breaths heavily and the removal of carbon (IV) oxide causes this shift during exhaling. At the same time, the respiration problems make the lungs demand a lot of oxygen which would make the dissociation curve shift leftwards. When ARDS becomes worse, most of the tissues wear out, and some of the organs fail to perform. In this case, the lungs are worn out which affects the breathing rate (Kovach, 2014). As a consequence, the amount of carbon IV oxide increases and respiratory acidosis ensues. The resulting oxyhemoglobin dissociate swing is to the right again.

Change of Events Suitable to Minimize the Likelihood of Suffering from ARDS

One of the change events to adopt in this case is the identification of individuals that are susceptible to suffering from ARDS. Identification of such patients is necessary to ensure that such problems are detected and treated at an early stage. Therefore, immediately the patient was diagnosed with breathing problems, an ARDS service provider would have been notified to initiate treatments. The patient showed they exhibited distress in her breathing and this should have sent a signal that the patient needs specialized care. Immediately, an X-Ray was crucial to help detect the chest problems and the detrimental effects that had destroyed the lungs and the alveoli. After the ray, there is a high-tech that would enable the patient to be treated for this syndrome. In addition, a non-invasive test on the exhaled air is also a suitable mechanism to help identify what the patient was suffering from. Therefore, the patient would have been subjected to a series of tests to determine the leading cause of respiratory difficulties.

References

Kovach, T. (2014, November 25). Oxygen-Hemoglobin Dissociation Curve [Video file]. Retrieved from https://www.youtube.com/watch?v=StpQmmuVnTA

McCance, K. and Heuthers, S. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th Ed). Maryland Heights, MO.: Mosby, Inc.

Sarkar, M., Niranjan, N., & Banyal, P. K. (2017). Mechanisms of hypoxemia. Lung India: official organ of Indian Chest Society, 34(1), 47.

Sharp, C., Millar, A. B., & Medford, A. R. L. (2015). Advances in the understanding the pathogenesis of acute respiratory distress syndrome. Respiration, 89(5), 420-434.