ARDS Acute Respiratory Distress Syndrome Amanda Burr Lauren Burgess Whitney Stevens Approximately 190,000 Americans are affected by ARDS annually. Up to 30% of ARDS cases can be fatal improvement from the 50%-70% death rate just 20 years ago. Patients who develop ARDS due to trauma or a lung infection usually do better than those who develop the condition due to sepsis (infection of the blood). Ranges from1.5 to 75 cases per 100,000 persons Statistics Occurs when fluid builds up in the alveoli of the lungs. With increased fluid, less oxygen can rech the bloodstream. Organs become oxygen deprived. Indirect Shock Sepsis (bacterial infection of the blood) Trauma Multiple blood transfusions MODS Direct Breathing in salt water Breathing in harmful smoke or fumes Breathing vomit into the lungs Narcotics Sedatives Overdoses of tricyclic antidepressants Pneumonia or other lung infection Causes Symptoms Severe shortness of breath. Usually develops within a few hours to a few days after the original disease or trauma. Risk of death increases with age and severity of illness. Survivors may recover completely Lasting lung damage can occur. Symptoms Labored and unusually rapid breathing Low blood pressure Confusion and extreme tiredness ARDS usually follows a major illness or injury Most patients are already hospitalized. Causes Bacteremia Sepsis Trauma, with or without pulmonary contusion Fractures, especially multiple fractures and long bone fractures Burns Massive transfusion Pneumonia Inhalation of harmful substances Head, chest or other major injury Aspiration Drug overdose Near drowning Postperfusion injury after cardiopulmonary bypass Pancreatitis Fat embolism Risks People with history of chronic alcoholism are at higher risk of developing ARDS They are also more likely to die from ARDS ARDS is a prominent manifestation of Multiple Organ Dysfunction Syndrome (MODS) MODS occurs when the organ systems fail Acute respiratory distress syndrome (ARDS) is a rapidly progressive disorder that initially manifests as dyspnea, tachypnea, and hypoxemia, then quickly evolves into respiratory failure. Because the presenting symptoms of ARDS are nonspecific, physicians must consider other respiratory, cardiac, infectious, and toxic etiologies Patient history (i.e. comorbidities, exposures, medication) in conjunction with a physical examination focusing on the respiratory and cardiovascular systems can help narrow the differential diagnosis and determine the optimal course of treatment. Difference in diagnosing CHF and ARDS Congestive heart failure is characterized by fluid overload Patients diagnosed with ARDS, by definition, do not show signs of left atrial hypertension or overt volume overload. Patients with congestive heart failure may have edema, jugular venous distension, third heart sound, an elevated brain natriuretic peptide level, and a salutary response to diuretics. Distinguishing between Pneumonia and ARDS a patient with uncomplicated pneumonia may have signs of systemic and pulmonary inflammation (i.e., fever, chills, fatigue, sputum production, pleuritic chest pain, and localized or multifocal infiltrates); accompanying hypoxia should respond to oxygen administration. If hypoxia does not correct with oxygen administration, ARDS should be suspected and confirmed based on AECC diagnostic criteria. In those with combined pneumonia and ARDS, treatment entails antibiotics and ventilator management. Physical ARDS may cause abnormal breathing sounds, such as crackling. signs of extra fluid in other parts of your body. Extra fluid may mean there are heart or kidney problems. bluish color on skin and lips Initial Tests An arterial blood gas test. This blood test measures the oxygen level in your blood using a sample of blood taken from an artery. A low blood oxygen level might be a sign of ARDS. Chest Xray Blood Tests Other Tests Chest computed tomography Heart tests that look for signs of heart failure. Pathophysiology ARDs is characterized a sudden respiratory failure. Clinical signs of ARDS can be seen within the first few hours: dyspnea, tachypnea, pallor, diaphoresis. an increase in the use of the accessory muscles, including the internal intercostal muscles, pectoralis major, scalene, trapezius and the sternocleidomastoid muscles. Pathophysiology Injury to the vascular system of the lungs is typically the most significant cause of ARDs Neutrophils are then seen to accumulate in the area of injury. There they release toxic mediators such as pro inflammatory cytokines, reactive oxygen species, proteases, and procoagulant molecules. Essentially, it is a large inflammatory response. Pathophysiology While injury to the epithelium of the lung causes damage, it is the harm done to the alveoli that causes the biggest problem Neutrophils migrate from their residence in the lung epithelium and move into the air spaces. From there they continue their course into the epithelium of the alveoli. The Exudative Phase In this phase, one experiences hypoxemia due to the pulmonary edema in the alveoli. The large number of neutrophils release toxic molecules that can destroy the tight junctions and induce apoptosis of the type I and type II alveolar cells As the Type II cells are destroyed, surfactant production in decreased which leads to the collapse of the alveoli. This is the point at which mechanical ventilation (which will be discussed later) would be used. Increasing complications in this phase The increase in pulmonary resistance leads to hypertension which can lead to right ventricular failure The next phase. If ARDS is not resolved in the first week, a patient can enter the fibroproliferation phase. During this period, the patient can develop fibrosing alveolitis, or inflammation between the fibrous tissue between the alveoli and the lung that causes fibrogenesis. This creates a closely woven tissue that isnt as elastic. That poses a problem when trying to breathe, doesnt it. The resolution phase The next phase is the resolution phase. At this times the lungs are returning to their normal histology. While much of this stage remains unclear, researchers have seen the epithelium become repaired and the neutrophils undergo apoptosis. The edema is the lungs is transferred from the alveoli into the lung interstitial and the protein is removed. The fibrotic changes that occur also require remodeling but little is known about this process. There is still so much that we dont know Acid Base Disorder Often present in patients Acid-base homeostasis involves the lungs, the kidneys and endogenous buffers. Normal Body pH is 7.4 Buffers Buffering is the ability of a weak acid and its corresponding base to resist change in the pH upon the addition of a strong acid or base Principle buffer in the body is the carbonic acid/bicarbonate base. Almost all of the carbonic acid in the body exists as carbon dioxide. However, the concentration of acid or base in your blood can reach levels which exceeds buffering capacity. The Role of the Kidneys This is considered the metabolic parameter. The primary role of the kidneys in this system is to regulate the concentration of bicarbonate, which is a base. HCO3 binds with the free H+ to reduce its concentration Bicarbonate is reabsorbed in the proximal tubule Metabolic Acidosis Metabolic acidosis is considered a blood pH of 7.45 PaCO2> 26 In order to answer those questions we can use a tic-tac-toe chart organize what we know AcidNormal Alkaline We fill out this chart using the our patients Arterial Blood Gas (ABG) results, which include the pH, PaCO2, and HCO3 like we saw on the last chart. Patient: RM pH: 7.26 PaCO2: 33 HCO3: 17 AcidNormalAlkaline pH< >7.45 PaCO2> 26 AcidNormal Alkaline pHPaCO2 HCO3 So, this means that he is in a state of acidosis because of a decreased level of bicarbonate. We see that his PaCO2 is more alkaline than what is normal. What does this mean? Metabolic acidosis with respiratory compensation Now for one on your own Patient: LR pH: 7.48 PaCO2: 31 HCO3: 21 AcidNormalAlkaline pH< >7.45 PaCO2> 26 AcidNormal Alkaline Medicine to prevent and treat infections and to relieve pain Oxygen Therapy & Support Ventilation Tracheostomies ( incision in the windpipe) Lung transplants or cardiopulmonary transplantation MNT Treatment of underlying disease or trauma Intervetions Codicote steroids to decrease inflammation and immune response and WBC movement into alveoli Prednisone Antibiotics Prevent Sepsis MODS Diuretics Control fluid levels Immunosuppressants To decreases inflammation Blood pressure supporting medications Dopamine Neosynephrine Medications Too much CHO Stress on lungs due to increase O2 needs Too much fluid Blood thinners Decreases blood pressure Medications & Things to Avoid Nasal cannula: Oxygen through tubes in your nose or through a mask Supplemental oxygen Ambulatory Non-invasive Oxygen Therapy & Support When? When lungs are no longer able to work on their own Why not immediately? Ventilation causes atrophy of the lung muscles and other complications Goal? support the patients breathing during the time needed for the lungs to recover Get carbon dioxide out of the body Machine Ventilation Mechanical ventilator: Oxygen through a breathing tube. The tube is flexible and goes through your mouth or nose into your windpipe. The tube is connected to a ventilator The ventilator does the actual breathing for you or assists you in breathing What is it? Mechanical Ventilator The patient is connected to the ventilator by a tube, which goes through their mouth or nose to the trachea. This tube (referred to as an endotracheal tube) passes through the vocal cords https://www.youtube.com/watch?v=V8VIw0fk4X0 How Does It work? Preliminary results from a study by the National Heart, Lung and Blood Institute suggested that receiving small, rather than large, breaths of air from a mechanical ventilator reduced the number of deaths by 22 percent and increased the number of days without ventilator use. WHY DO YOU THINK THAT IS? Baby lung Studies Respiratory muscle weakness Retention of CO2 Patient is unable to speak due to tube blocking vocal chords Pt put on sedatives and pain medication Ativan or Versed Risk of infection Pneumonia Coughing risk to irritate lungs Problems with Ventillation Pneumothorax What is it? Air leaks out of the lungs into the space between the lungs and the chest wall Problems? Pain, shortness of breath, and lungs can collapse Cause? Forced airflow Other Risks of Ventilators Cystic Fibrosis Emphysema Medically compromised Malnourished Older Increase Risk Fatcors Enteral Feeding Until the patient can eat again by mouth, food is given into the stomach or intestine through a feeding tube by enteral nutrition. If liquid feeding is required for longer than one or two weeks, a surgical procedure may be performed to place a tube through the abdominal wall directly into the stomach or intestine (G-tube, J-tube, or PEG). Parenteral Feeding Given if the esophagus is obstructed and feeding cannot be done enterally Feeding on Ventilation How feeding works Pulmonary PEPTAMEN AF Helps with inflammatory response and GI absorption/ high protein/ antioxidants Oxepa Calorically dense/ helps inflammatory response Enteral Formulas Kcal/mlProtein (g/L)CHO (g/L)Fat (g/L)mOsmFree H2O (mL/L) 1.PSU (HBE) = HBE(.85) + Tmax(175) + Ve(33) 6344 (mechanically ventilated, non-obese, critically ill patients) 2.PSU (HBEa) = HBEa(1.1) + Tmax(140) + Ve(32) 5340 (mechanically ventilated, obese, critically ill patients) 3.PSU (m) = Mifflin(0.96) + Tmax(167) + Ve(31) 6212 (most precise expect for obese elderly) Energy Requirements on Ventilation Tmax = maximum body temp in 24 hours Ve = expired minute ventilation Tracheostomies What is it? A breathing tube, also called a trach tube, is put through the tracheostomy and directly into the windpipe to give more oxygen from the ventilator When? Usually done 14 days after ventilation and if patient will be on ventilation for a couple of weeks How long? Usually temporary until off the ventilator but can be permanent Tracheostomies Why? Patient is unable to do the nasal or oral route for mechanical ventilation Patient is sensitive to coughing Patients with swallowing problems Risks Infection Feeding Enteral Parenteral Oral Tracheostomies Lung Transplants Some double lung transplants have been successful Risks? GVHD Can cause ARDS Why? Complete lung failure Lung Transplants Factors Underlying disease, age, and prior nutrition status Increase caloric needs Due to hypercatabolism or hypermetabolism Cautions Malnourishment and underweight MNT Indirect calorimetry measurements Anthropometric measurements Labs can be thrown off Fluid imbalances, mediations, and ventilator support Immunocommpetence Chronic mouth breathing Aerophagia Swallowing too much air Dyspnea Difficulty or labored breathing Depression Exercise tolerance Nutritional Assessment Meet basic nutritional requirements Preserve LBM Restore respiratory muscle mass and strength Maintain fluid balance Improve resistance to infection Facilitate weaning form oxygen support and ventilation Low CHO Goals Energy needs are elevated Hypercatabolism and hypermetabolism from immune system Do not overfeed What are some problems/complications of overfeeding? Increase oxygen demand & increase CO2 in the body that the body cannot get out Energy Requirements best determined by continuous assessment due to fluctuation DAILY MONITORING IS CRUCIAL PEN Equations Indirect calorimetry is the gold standard O2 and Co2 are measured by breathing into a mouthpiece The Weir equation and respiratory quotient value 0.85 constant is used If conditions are met IC can be used on ventilated patients Energy Requirements This study looked at low energy permissive underfeeding (trophic feeding) vs. full energy enteral feeding (full feeding) effects on physical function, survival, and multiple secondary outcomes At 6 months there was no difference At 12 there was no difference Study: Trophic vs. Full Feeding Influenced by Organ system decompensation inability to compensate the load created by the disease Respiratory status Ventilation methods Nonprotein calories are divided evenly between fat and CHO CHO & Fats Increase protein needs due to negative nitrogen balance WHY? Not using their muscles = LBM breakdown and trauma/sepsis/inflammation/underlying disease Calculated 1.5 to 2 g/kg body weight Protein Exact requirements are unknown Supply to DRI plus repletion Those with antioxidant, healing, immunity and anabolism functions may be increased Vitamin E & C, Selenium Electrolytes are monitored closely Fluid imbalances Respiratory acidosis or alkalosis K+, Ca, Mg loss in urine due to medications Vitamins & Minerals Too much fluid will fill the lungs Not enough fluids will limit blood flow to organs = decrease in oxygen to organs Usually given intravenously Carefully monitored Diuretics are used to maintain fluid balance Fluids Small portions of favorite foods If not ventilated or has tracheostomy Intubated Enteral feeding or parenteral Feeding Methods Anorexia Early satiety Malaise (discomfort or illness) Bloating Constipation diarrhea Feeding Complications From Low Oxygen Supportive breathing technique called positive end expiratory pressure (PEEP) Noninvasive positive pressure ventilation (NPPV) Wear a mask connected to a device that uses mild air pressure to keep your airways open while you sleep Rocking bed A mattress on a motorized platform rocks back and form as you sleep Alternative Therapy