ARDS: Acute Respiratory Distress Syndrome (PDF)

Critical Care Nursing Program Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Introduction Acute Respiratory Distress...

Critical Care Nursing Program Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Introduction Acute Respiratory Distress Syndrome (ARDS) is an exemplar that illustrates more key concepts of inflammation. Acute respiratory distress syndrome (ARDS) causes diffuse alveolar capillary (A-C) membrane damage. It is a restrictive process which results in decreased vital capacity (VC) and residual volume (RV) causing alveolar collapse and, in turn, decreased compliance and subsequent refractory hypoxemia. ARDS is viewed as an elusive phenomenon as it is difficult to define, diagnose and treat. ARDS accounts for 10% of global ICU admissions (Bellani et al, 2016). Despite continuous attempts being made to improve the outcome for patients with ARDS, mortality rates remain at approximately 24-48% (Griffiths et al., 2019). Learning Outcomes On completion of this unit, the learner will be able to: 1. Discuss the phenomenon known as Acute Respiratory Distress Syndrome (ARDS). 2. Describe the etiologies, pathophysiology, assessment findings, diagnostic evaluation and management strategies associated with ARDS. Required Reading Please refer to your reading list for Inflammation I Etiology of ARDS ARDS is triggered by an insult to the body, which initiates alveolar capillary membrane damage. The risk of developing ARDS increases proportionately with the number of precipitating factors occurring. The risk factors for ARDS are listed in your required readings. The most common precipitating factors for developing ARDS are sepsis, pneumonia, trauma and aspiration of gastric contents. Because the mechanism causing the alveolar capillary membrane damage is so poorly understood, there is no Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 1 of 9  Critical Care Nursing Program method by which to predict which patient, subjected to these etiologies, will develop ARDS. It is therefore essential to closely monitor any patient who presents with the predisposing factors for ARDS which evolves from an underlying inflammatory process. Review of Normal Physiology A review of a few aspects of normal physiology will help you understand the pathophysiology of ARDS. The key concept is normal capillary fluid dynamics and how this relates at the alveolar-capillary membrane. Alveolar-Capillary membrane The alveolar epithelial cells serve as the principal protector against alveolar fluid accumulation because they attach to each other, overlap and, unlike the alveolar endothelial cells, form tight junctions. Also, the interstitial pressure gradient favours the movement of fluid away from the alveolar wall so that it may be drained by the lymphatic system. This illustrates why interstitial edema precedes alveolar edema. Although fluid leaks into the interstitium, it will not accumulate and result in gas exchange abnormalities because it is removed adeptly by the lymphatic system. Consequently, the alveoli will flood only if the rate of fluid filtration increases beyond the capability of the lymphatics to drain it away. Pathophysiology of ARDS ARDS causes diffuse alveolar-capillary (A-C) membrane damage. The damage to the alveoli results in injury to the two types of epithelial cells: Type I and Type II. Type I cells, responsible for gas exchange, are thin and cover 90% of the surface area of the lung. These cells lie close together and form a watertight surface, which, under normal conditions, prevents interstitial fluid from entering the alveoli. These cells are very susceptible to injury and have limited restorative capabilities. The remaining 10% of the surface area of the alveolar barrier is covered by the more compact Type II cells which secrete surfactant, the product that decreases alveolar surface tension. These cells seem to be less susceptible to injury and have outstanding reparative capabilities (Ballast, 2000; Schlenker, 2002). When the A-C membrane is damaged it becomes more permeable and, as a result, fluid and particles leak out of the capillaries into the interstitial fluid compartment and subsequently into the alveoli. This is known as noncardiogenic pulmonary edema, also called a low-pressure pulmonary edema. With this type of pulmonary edema, the alveolar capillary membrane is damaged and thus becomes more permeable. Consequently, plasma proteins and even some red blood cells move into the Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 2 of 9  Critical Care Nursing Program interstitium. This loss of plasma proteins from the vascular space reduces the vascular colloidal osmotic pressure. Subsequently, because of the interstitial protein, fluid is pulled out of the vasculature and into the interstitium. The fluid cannot move back into the intravascular space because of the low colloidal osmotic pressure. This, in turn, leads to pulmonary edema. However, unlike cardiogenic pulmonary edema, non- cardiogenic pulmonary edema has a normal pulmonary capillary hydrostatic pressure. As a result, ARDS is referred to as a low-pressure pulmonary edema. When the watertight barrier is lost with the alveolar damage, fluid, protein, and debris (erythrocytes, leukocytes, and fibrin) enter the alveoli causing alveolar edema and alveolar collapse. The protein and debris form into sheets producing a hyaline membrane, which causes a diffusion defect. Damaged Type I cells are replaced by thicker cells. Damage to Type II cells causes a decrease in surfactant leading to alveolar collapse. Signs and Symptoms Associated with ARDS Hypoxemia with its related physiologic responses is a major feature of ARDS. Depending on the initial insult responsible for ARDS, signs and symptoms of the underlying disease process may also be present. If you attempt to use the table describing physical assessment findings according to the stage of ARDS in your readings, you will find yourself being confused so don’t try to memorize that table. The points to remember are: 1. The patient may or may not pass through all three phases associated with ARDS and the ARDS may resolve at any time. 2. The onset (first 12 hours) is subtle and often missed. 3. Within 12 -24 hours signs and symptoms are more obvious. 4. At 24-48 hours it becomes obvious that the patient is in respiratory failure. Please refer to your reading list for Inflammation I Clinically, patients will not be classified accordingly to their stage (i.e. in report you will not hear someone say “this patient is in the fibroproliferative phase of ARDS”), however it is important to understand the pathophysiology and associated signs and symptoms of each stage as it will determine the patient’s treatment. Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 3 of 9  Critical Care Nursing Program Case Study: Roger Parker Roger Parker is a 58-year-old, white, able-bodied, self-identified male with a history of chronic alcoholism, malnutrition, and hypertension. He was originally admitted to ICU with acute pancreatitis and pleural effusions. Now on day 3, his breathing is laboured (RR 32), he is on a NRB 100% with a PaO₂ 50. His abdomen is grossly distended; his pain is so significant he had to be placed on a Fentanyl/Sublimaze infusion and CXR shows bilateral infiltrates and an existing pleural effusion. The healthcare team is preparing for intubation. Diagnostic Evaluation Methods ARDS can be difficult to identify in the early stages as symptoms are often subtle or are assumed to be caused by other disease processes. The Berlin Definition of ARDS is often used as diagnostic criteria by health care practitioners and consists of four main criteria: timing, imaging, origin of edema, and oxygenation. ARDS is often described as refractory hypoxemia and therefore the severity of ARDS is often based on the patients PaO2/FiO2 ratio. The following diagram outlines the Berlin Definition of ARDS and early management techniques that should be implemented in patients that are diagnosed with ARDS depending on the severity of the disease. The P/F ratios outlined are helpful in assessing whether the patient is experiencing mild-severe ARDS. Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 4 of 9  Critical Care Nursing Program (Adapted from Papazian et al., Annals of Intensive Care 2019; 9(1): 1-18) Although historically, and as outlined in the Berlin Diagnostic Criteria for ARDS, chest radiography has been an integral part in the diagnosis process of this disease. The use of Lung Ultrasound (LUS), however is becoming more common in diagnosing this disease. LUS is a non-invasive procedure that does not expose patients to ionizing radiation that chest radiography and computerized tomography (CT) does. LUS can be used to assess decreased aeration and consolidation in the lungs to assist in determining the severity of ARDS (Sanjan et al., 2019). Although this is not a skill a Critical Care nurse will be responsible for, as the role of Point of Care Ultra Sound (POCUS) continues to be more prevalent in the ICU settings, this method may be used in the assessment of ARDS and the associated severity and therefore may require the assistance of the assigned nurse. As with any other assessment tool, always remember to put the patient’s puzzle together and include patient history, presentation, physical assessment and signs and symptoms to make the most accurate diagnosis. Management Strategies Please refer to your reading list for Inflammation I Module #7: Inflammation I Unit #3: Inflammatory Processes - Acute Respiratory Distress Syndrome (ARDS) Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 5 of 9  Critical Care Nursing Program “Despite the tremendous amount of research into the prevention … of ARDS, there is currently no generally agreed-upon therapy that prevents the development or progression of lung injury or promotes lung healing once injury is established” (Darovic, 2002, p. 463). Treatment goals for the patient with ARDS include removal or control of the underlying problem, maintenance of pulmonary oxygenation, and optimization of oxygen delivery to the tissues. Treatment of the underlying cause varies depending on the precipitating cause. Supportive measures are aimed at promoting gas exchange, supporting tissue perfusion, and preventing complications. Promote Gas Exchange Treatment strategies to promote gas exchange in the patient with ARDS include: ventilatory support, decreasing O2 consumption and metabolic O2 requirements, fluid management, prone positioning and nutritional support. Ventilatory Support There is no supporting data that acknowledges the superiority of any particular ventilatory support mode in the treatment of ARDS. However, the guiding principles are uniform (Do no harm): utilize the lowest level of oxygen possible to support tissue oxygenation and accomplish this with minimal barotrauma and hemodynamic compromise. Remember back to the concepts of ventilation and oxygenation as it will help you decipher how normal physiology has been altered with this disease process. The following are some ventilatory strategies that you may see being implemented with your patient: The best amount of PEEP in ARDS remains uncertain (Fan et al., 2017). PEEP should promote maximal PaO2 while minimally decreasing cardiac output. PEEP is used to recruit areas of the lung that have collapsed with ARDS. The level of PEEP is increased while the difference between the plateau pressure and the PEEP is measured. For patients diagnosed with moderate to severe ARDS, high levels of PEEP may be used as recruitment strategies as well as to decrease intrapulmonary shunts in attempts to increase arterial oxygenation. High levels of PEEP should only be used in patients in which oxygenation improvements are noted, are hemodynamically stable, and maintain Pplat