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UT Arlington NURS 5315 - Acute Respiratory Distress Syndrome in the Human Body

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Running head: ACUTE RESPIRATORY DISTRESS SYNDROME 1Acute Respiratory Distress Syndrome in the Human Body The University of Texas at Arlington College of NursingIn partial fulfillment of the requirements of N5315 Advanced PathophysiologyJohn D. Gonzalez DNP, APRN, ACNP-BC, ANP-CFebruary 23, 2019ACUTE RESPIRATORY DISTRESS SYNDROME 2 Acute Respiratory Distress Syndrome in the Human BodyThis paper will break down the process of an individual coming in through the ER andwhich respiratory disorder is taking place. The presented scenario will be broken down intoseveral questions and describe why the patient is believed to have Acute Respiratory DistressSyndrome (ARDS). The evidence will support why this is the answer and what could thenhappen to the patient if correct interventions are not acted on. Question 1: The clinical scenario is most consistent with which diagnosis? - Acute Respiratory Distress Syndrome (ARDS)Question 2: What data in the clinical scenario supports your diagnosis?- Dyspnea - Tachypneic (respiratory rate of 30 breaths/min) - Febrile (39 degrees Celsius) - 102.2 degrees Fahrenheit - WBC Count 20,000 - Hypoxic (low oxygen saturation 89%) - Chest x-ray film reveals infiltrate in both lower lobes - Intubation and Ventilatory support - Arterial blood oxygen level remaining low despite mechanical ventilation Question 3: What caused the development of the diagnosis you identified in question 1? - Pneumonia - Becoming Septic with fever and high WBC count Question 4a: What are the common causes of the disorder you identified in question 1? Although it is not clear why some people will develop ARDS and others won’t there are a few predisposing factors of those that will develop ARDS. Some of the factors included are geneticACUTE RESPIRATORY DISTRESS SYNDROME 3factors, sepsis, and multiple trauma (especially when multiple transfusions are received). Other causes of ARDS may include pneumonia, smoke or noxious gas inhalation, oxygen toxicity, radiation therapy, burns, aspiration, cardiopulmonary bypass surgery, pancreatitis, disseminated intravascular coagulation, and drug overdose. (Brashers, 2019, p. 1175)Question 4b: What are the main pathophysiologic factors in the disorder you identified in question 1, that cause the accumulation of extravascular fluid in the lungs? When ARDS occurs, massive inflammation occurs in the alveolocapillary membrane which then causes alveolar flooding with protein-rich fluid leading to severe pulmonary edema. Therefore, the patient continued to worsen despite treatment because the fluid continued to accumulate in his lungs. (Brashers, 2019, p. 1175)Question 4c: What accounts for the severe hypoxia associated with the disorder identified in question 1, despite using high oxygen levels and mechanical ventilation?The severe hypoxia is due to the lungs filling up with fluid and the patient unable to obtain enough oxygen even while on mechanical ventilation due to the pulmonary edema. The increase in pulmonary edema causes a V/Q mismatch which reduces the lungs ability to function correctlyultimately leading to hypoxemia. (Brashers, 2019, p. 1175)Question 4d: What is an A-a gradient and what would you expect this patient’s A-a gradient to be? The Alveolar – arterial gradient (A-a gradient) is the difference between the alveolar concentration of oxygen (PAo2) and the arterial concentration of oxygen (Pao2) which describes whether there has been equilibration of O2 between alveolar gas and pulmonary capillary blood. In this patient with ARDS the A-a gradient would be widened or increased (greater than 20 mmHg and less than 10 mmHg) because the equilibration of O2 is impaired (Costanzo, 2018, pp.ACUTE RESPIRATORY DISTRESS SYNDROME 4239 - 240). A patient with ARDS would have a PF ratio of < 300 mmHG which would be used todiagnose the severity of the patient’s disease. (Brashers, 2019, p. 1175)Question 5: For what actual or potential complications related to the diagnosis in question 1 does she need to be monitored? - Increased dyspnea- Increased hypoxemia - Increased infiltrated in lungs- Hyperventilation- Respiratory Alkalosis- Hypercapnia- Metabolic Acidosis- Decreased Tidal Volume- Organ dysfunction- Decreased cardiac output – hypotension (Brashers, 2019, p. 1175)ReferencesBrashers, V. L. (2019). Structure and Function of the Pulmonary System. In K. L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 1174-1176). St Louis, MO: Mosby Elsevier. Costanzo, L. S. (2018). Physiology (6th ed.). Philadelphia, PA: Elsevier.ACUTE RESPIRATORY DISTRESS SYNDROME


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