Acute Respiratory Distress Syndrome (ARDS) - Professor Salazar PDF

1 Hi, MS3. My name is Professor Salazar, and today we're going to be reviewing the exemplar of acute respiratory distress syndrome, otherwise known as ARDS. The concept for this exemplar is ox...

1 Hi, MS3. My name is Professor Salazar, and today we're going to be reviewing the exemplar of acute respiratory distress syndrome, otherwise known as ARDS. The concept for this exemplar is oxygena on. 2 ARDS can be classi ed by a number of things, including its rapid onset, non-cardiac pulmonary edema and refractory hypoxemia, which means that the arterial oxygena on is low despite adequate oxygena on being administered or inspired. ARDS is also characterized by lung ssue in amma on, which will appear as bilateral in ltrates on a chest X ray, small blood vessel injuries, and it results in mul organ dysfunc on. It is o en caused by pneumonia, sepsis, aspira on or severe trauma. 3 In this slide, we are looking at a side-by-side X-ray of a pa ent with a normal chest X ray versus a pa ent with ARDS. X-ray to the le is a pa ent with ARDS, and you can tell this by the whited out nature of the bilateral lung elds. On the right, you can see that the bilateral lung elds are grayed, dark black in certain areas, and this is how air is exposed on the X ray. The higher the density, the whiter the color, and the lower the density, the darker the color. On chest X rays to the le , you can see that this pa ent's lung is full of atelectasis, in ltrates and edema, and there's very li le air in the lungs, and decreasing the ability for gas exchange that needs to occur in this lung. 4 ARDS can have a pre y complex pathology. Normally, ARD starts with a systemic in ammatory immune response, be er known as SIRS. This is a chemical mediated in ammatory response that occurs because of the ac va on of the pa ent's immune system, basically wreaking havoc on the body, causing more permeable membranes, plasma leaking into body systems, decreased blood pressure and increased heart rates, the SIRS response ul mately leads to the alveoli and the capillary membrane being damaged. When this occurs, plasma and blood leak into the inters al space of the lungs and eventually enter into the alveoli. When the uids enter the alveoli, it causes damage to the surfactant producing cells. Surfactant, if you remember, is a chemical produced by the body that allows the alveoli to stay open like an in ated balloon and not get stuck together when the pa ent exhales. This allows for gas exchange to occur even during exhala on, when alveoli collapse occurs. It can lead to atelectasis fi fl fl ti ti ti ti ft fi tt fi ti ti tt fi ti ti fl ti ft ti ti ti fi ti ti ti ft fl ti ti ti ti ti tt fl  5 As ARDS con nues to evolve. It creates decreased lung compliance and impaired gas exchange. Lung compliance tells you how s or elas c a lung is and how hard the ven lator has to work to allow the lung to in ate for the gas exchange to occur. Hypoxia becomes resistant to oxygen. It doesn't ma er how high I turn up my FiO2, the pa ent's SPO2 and PAO2 are going to remain unchanged. PaCO2 rises as di usion is further impaired. PaCO2 is the amount of carbon dioxide in the pa ent's blood, and it's increasing because there are not enough sites for gas exchange to occur. A hyline membrane forms that further reduces gas exchange and further decreases lung compliance, and then ul mately, bro c changes in the lung leave less surface area for gas exchange to occur. and the use of mechanical ven la on increases that mortality to 65.7 to 94% there are a number of risk factors that have shown to increase the chances of developing arts. However, it s ll remains uncertain as to who and why ARDS occurs most. 6 Pa ents who develop acute respiratory distress syndrome, syndrome are typically hospitalized. Factors that may increase their risk of developing ARDS include age greater than 65 a history of tobacco use, alcoholism, chronic lung disease, immunosuppression and exposure to air pollu on, factors that will increase the risk in a pa ent with covid, 19 include advanced age, diabetes and hypertension, ARDS develops in almost 42% of pa ents presen ng with covid pneumonia, and 61 to 81% of those pa ents require intensive care admissions. 7 Some direct lung injuries increase the risk of occurrence of ARDS. These include aspira on pneumonia, pulmonary infec ons from pneumonia or viral infec ons, including those associated with covid 19 inhala on injuries from burns or saltwater near drownings and pulmonary contusions. 8 Non direct lung injuries that can increase the risk of ARDS include sepsis, mul ple traumas, acute pancrea s, drug overdose, mul ple blood transfusions, cardiopulmonary bypass surgery and major burns because of the uid shi s that occurred occur with burn injuries. 9 The best way to treat ARDS is to prevent arts. We need to iden fy and prevent risk factors that can increase the chances of ARDS. We can put pa ents on aspira on precau ons. We can ini ate early uid resuscita on and an bio cs for sepsis and making sure that we use appropriate precau ons for immunocompromised pa ents, we can also assess for the presence of early warning signs which can occur, including the increasing need of oxygen and the decrease in ac vity tolerance. ti ti ti ti ti ti ti ti ti ti ti ti ti fi fl ti ti ti ti ff ti fl ti ti ti ti tt ti ti ti ti ti ti ti ti ti fl ti ft ti ti ti ti ff  10 The onset of early symptoms typically occur within the rst 24 to 48 hours a er insults. This is true for direct or indirect lung injuries. One of the rst signs of hypoxia is o en changes in mental status. The pa ent can o en become confused and restless. This is associated with high levels of PACO2, dyspnea or shortness of breath and tachypnea, which is increased respira ons are clear signs of early ARDS, as well as an increased pulse and an increased temperature. Breath sounds may be normal, or they may be ne with sca ered crackles, mild hypoxia occurs, crea ng respiratory alkalosis. This is because the pa ent begins to breathe more quickly because they're short of breath, and then they breathe o excessive amounts of CO2 in early stages, chest X rays and arterial blood glasses may show very li le signs of change, if any. 11 During the late stages of ARDS, you will see increased respiratory distress, including intercostal retrac ons and the use of accessory muscles, which are all referred to as increasing the work of breath. As pa ent's tachypnea, worse is as their demand for oxygen increases, Crackle and Ronchi develop with increased uid accumula on in the lungs. The chest X ray will show inters al changes in patchy in ltrates, which will show as a whi ng out of the lungs in the X ray. Pulse ox levels show refractory hypoxemia, and there's o en cyanosis present and increased agita on, confusion and or lethargy. 12 The Berlin de ni on is a way we classify ARDS. It can tell us about the severity of the pa ent's ARDS, and it's directly associated with their mortality using a PF ra o. When assessing a normal PF ra o, it is normally 400 to 500 milligrams of mercury. In mild ARDS, the number will stay between 200-300. ARDS is considered to be moderate when that number stays between 200- 100 and then pa ents with the PF of less than 100 are considered to be in severe ARDS and have the highest mortality. A PF ra o is the ra o of arterial oxygen, par al pressure, PAO2 to frac onated inspired oxygen, FiO2. The normal PF ra o is approximately 400 to 500. The math here is fairly simple to determine the PF ra o, but you must make sure that you are using a decimal and not percentage for the FiO2. Let's say that a pa ent's PAO2 is 90 and they are on an FiO2 of 40 percent. You would simply divide 90 by point four for an answer of 225. 225, would be mild, a mild case of ARDS, compared to a regular person who , ideally has a PAO2 of 100 and is on room air, which is approximately 21% oxygen. So if you do the math there 100 divided by 0.21 is 476, and this is within your normal PF values. 13 This is another great overview of the symptoms of a pa ent with ARDS. Signs and symptoms include tachypnea, dyspnea, accessory muscle use hypoxia, tachycardia and a decreased pulmonary compliance. ABGs will show a decrease in the PAO2, even though there is an increased FiO2 and then the cause of ARDS, include trauma, pulmonary infec on, aspira on, prolonged cardiopulmonary bypass, shock, fat emboli and sepsis. ti ft ti fi fi ti ti ti ti ti ti ti ft tt ti ti ti ti ff ti ti ti ti ti ft ti tt fi ti ti fl fi ti ti fi ti ft ti ti  14 ARDS has three phases. Phase one is the Exuda ve phase, and typically occurs within the rst seven to 10 days is categorized by hypoxemia, requiring high concentra ons of oxygen and peep, pulmonary edema. O en the pa ents have crackles and a decreased surfactant produc on. In some cases, pa ents who do improve during this me are able to be weaned o the ven lator. 15 If the pa ent does not improve, they typically progress into phase two, which is the prolifera ve phase. And this occurs approximately seven to 14 days a er the start of ARDS progression. 16 There is an ongoing in ammatory response, resul ng in persistent hypoxemia, worsening chest X rays and having a decreased lung compliance, the pa ent will also have persistent ven lator dependence and pulmonary hypertension. The pulmonary hypertension is occurring because the lungs are so bro c, the heart is having to work harder to pump blood through the lungs to be oxygen oxygenated, and in turn, leads to right sided heart failure and pulmonary hypertension. 17 ARDS will eventually progress into phase three, the bro c phase, which happens weeks to months past the ini al lung injury. There's s ll chronic in amma on and brosis in the alveoli, but hypoxemia and in ltrates do eventually improve over these weeks and months, the pa ent is typically s ll dependent on long term mechanical ven la on, whether that means a tracheostomy or supplemental oxygen, not every pa ent progresses to this phase, and this phase is associated with an increase in mortality. As bedside nurses, we must support the pa ent and the family during this me. O en, survival rates are not high with this progression of the ARDS, and many mes, it leads to MODS, right sided heart failure decreases end organ perfusion, which will lead to mul organ dysfunc on syndrome, or MODS, which is the most common cause of an ARDS pa ent's death. If the pa ent does begin improving during this phase, it's o en over weeks and months, cardiopulmonary func on can return to near pa ent's baseline, but it can take up to six months or longer a er that ini al lung injury, many survivors of ARDS are le with lung func on de cits, cogni ve de cits, emo onal de cits and physical de cits. 18 Taking care of a pa ent with ARDS requires collabora on. The healthcare team will include nurses, respiratory therapists, physicians, pharmacists, die cians and physical therapists and occupa onal therapists. The nurse's primary focus will be on con nually monitoring the pa ent's condi on and responding to subtle cues and changes that occur in the pa ent. And in those cases, we will be intervening appropriately and are repor ng these changes to our care team. ti fi ti ti ti ti ti fi ti ti ft ti ti ti fi ft ti ti ti fl ti ti ti ti ti ti ff ti ti fi ft ti ti ti ft fi ti ti ti fi ti fi ti ti ti ti ti ti ti ti fi fl ti ft ti ft ti ti ti ti fi ti  19 In the next two slides, we will discuss some diagnos c tes ng that will point us to the diagnosis of ARDS, acute respiratory distress syndrome. ABGs can be analyzed to determine oxygen levels in the pa ent's blood, it will typically show hypoxemia and ini ally respiratory alkalosis, due to the pa ent breathing quickly and dumping their CO2. Over me, this is not sustainable, and the pa ent will not be able to blow o enough CO2, resul ng in respiratory acidosis. As the lung. Become more and more damaged, and the CO2 levels increase, metabolic acidosis can also be seen in pa ents with sepsis. Chest rays or chest CTS will both show bilateral in ltrates. 20 Other Diagnos c tests include CBC and blood chemistries. CBCs will watch for an uptrending in white blood cells, and in certain pa ents, thrombocytopenia may be seen. We will see increases in lac c acid, which tells us about anaerobic metabolism in the body. BMPs are cardiac markers which tell us about the strain of the heart. Blood cultures will be used to determine if the cause is bacterial sepsis. And then sputum cultures will also help us isolate bacteria or viruses that might be causing the lung injuries. Echocardiograms can be done, and they can tell us how the heart is responding to the changes in the lungs, and then EKGs will tell us speci cally about the electrical conduc vity in the heart. We can also view the lung with a bronchoscopy, which allows us to visualize the lung elds from the inside. Prolonged hypoxemia can lead to acute tubular necrosis and damage in the kidneys and can lead to liver damage. As a nurse, you'll want to assess kidney and liver func on closely. ti ti ti ti ti ti ti ti ti ti ti fi ti fi ti fi ti ff