Management strategies for ARDS include correcting hypoxemia and acid-base disturbance, restoring cardiac function, and treating the underlying disease or precipitating factors. This is generally accomplished with mechanical ventilation at 6-8 ml/kg ideal body weight and the application of PEEP to correct refractory hypoxemia. High levels of positive pressure may be required to produce adequate ventilation and oxygenation, but its adverse effect on cardiac function must be monitored closely. Some patients may benefit from pressure control (PC) ventilation to minimize the mean airway and parenchymal lung pressures. In PC mode the inspiratory time is increased and pressures are generally reduced, but the mean airway pressure may remain the same or slightly increased. This ultimately shortens the inspiratory time, inverts the I:E ratio, and potentially increases alveolar ventilation. As inspiratory time increases, and the elastic limit of the lung is reached, intrinsic PEEP increases air trapping and thus, may increase the PaCO2 while also increasing the occurrence of pneumothorax in an already stiff lung. These important considerations must be kept in fine balance with each factor receiving equal attention. More information about ongoing studies for ARDS can be found at www.ardsnet.org (Links to an external site.) Management of ARDS A multitude of causative factors may produce acute respiratory distress syndrome (ARDS). The clinical manifestations associated with ARDS usually appear within 6-72 hours of an inciting event, and worsen rapidly. The patient initially presents with dyspnea, cyanosis, bilateral crackles, tachypnea, tachycardia, diaphoresis, and use of accessory muscles on inspiration. A cough and chest pain may be present. The general clinical course is characterized by several days of hypoxemia that requires moderate to high concentrations of FiO2. The bilateral alveolar infiltrates and diffuse crackles are persistent during this period, and the patient’s overall health status is fragile as a result of the severe hypoxemia. Most patients who survive this initial clinical course begin to show oxygenation improvements and decreasing alveolar infiltrates over the next several days. Permissive hypercapnia, allowing the patient’s PaCO2 to increase, is used as a tradeoff to protect the lungs from high airway pressures. In most cases, an increased ventilator rate adequately offsets the decreased tidal volume used in the management of ARDS. The PaCO2, however, should not be permitted to increase to the point of severe acidosis (a pH below 7.2). Inverse Ratio Ventilation (IRV) IRV is a subset of PCV where the inflation time is prolonged, (In IRV, 1:1, 2:1, or 3:1 may be used. Normal I:E is 1:3). This lowers peak airway pressures but increases mean airway pressures. The result may be improved oxygenation but at the expense of compromised venous return and cardiac output, thus it is not clear that this mode of ventilation leads to improved survival. IRV’s major indication is in patients with ARDS with refractory hypoxemia or hypercapnia in other modes of ventilation. Prompt Case Study: Adult Respiratory Distress Syndrome History: Ms. Y is a 23 year-old woman who was feeling fine until the morning of admission when she began having severe chills, vomiting, diarrhea, headache, and fever of 40*C. The symptoms persisted throughout the day and caused her to seek medical attention at the local ED. Ms. Y had an intrauterine device (IUD) inserted at a local family planning clinic 3 days before admission. At the time of admission, she denied shortness of breath, wheezing, sputum production, cough hemoptysis, orthopnea, chest pain, illicit drug use, or exposure to TB. Physical Exam: -General Patient is well nourished, alert & oriented; she appears anxious but there is no evidence of respiratory distress -Vital Sign: Temp 40*C; RR 24 bpm; HR 104/min; BP 126/75 -Chest: Normal configuration & expansion while breathing; normal resonance to percussion bilaterally -Lungs: Clear to auscultation bilaterally -Abdomen: Lower abdominal tenderness to palpation -Extremities: No cyanosis, edema, or clubbing Lab Data: -CBC WBC 15,500 (high) Question #1 Does the patient appear to have a pulmonary problem at this time? Why or why not? Question #2 Does the patient’s medical problem predispose her to the development of ARDS? Ms. Y has been started on IV antibiotic therapy. Results of a uterine swab show gram-negative diplococci, and a preliminary blood culture also shows gram-negative cocci. Twelve hours later, she begins complaining of increased shortness of breath. Assessment: RR 34 bpm; HR 120/min She is using accessory muscles to breathe and chest auscultation now reveals fine, inspiratory crackles bilaterally. ABG: on RA -pH: 7.25 -PaCO2: 21 mmHg -HCO3: 16 mEq/liter -BE: -17 -PaO2: 62 mmHg -SaO2: 88% Question #1 What is the pt’s acid-base & oxygenation status? Interpret the blood gas and explain your answer. Question #2 What pathophysiology accounts for the adventitious lungs sounds (fine, inspiratory crackles)? The patient continues to experience severe respiratory distress and is placed on an air entrainment mask with a FiO2 of 60%. ABG on 60% FiO2: -pH: 7.26 -PaCO2: 35 mmHg -HCO3: 16 mEq/liter -PaO2: 49 mmHg Assessment: -RR 38 bpm -HR 134/min The chest film demonstrates an onset of diffuse bilateral infiltrates in the lower lobes; greater on the patient’s right side. Question #1 Interpret the ABG. Question #2 What initial settings would you place the patient on? Include mode of ventilation and indicate Why? Submit your answers in at least 500 words on a Word document. You must cite at least three references to defend and support your position.
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