Acute Respiratory Distress Syndrome Week 7 PDF

Summary

These notes cover the acute respiratory distress syndrome (ARDS), including explanations, types of respiratory failure, causes, and assessment. The material focuses on medical concepts related to respiration and the associated diseases.

Full Transcript

Acute Respiratory week 7 1. V/Q ratio- ratio should be 1:1 a. Imbalance V/Q is most common cause of hypoxemia b. V is ventilation= the amount of air that enters and leaves the alveoli c. Q is perfusion= amount of blood that flows to the alveolar capillaries, there m...

Acute Respiratory week 7 1. V/Q ratio- ratio should be 1:1 a. Imbalance V/Q is most common cause of hypoxemia b. V is ventilation= the amount of air that enters and leaves the alveoli c. Q is perfusion= amount of blood that flows to the alveolar capillaries, there must be enough blood passing through the lungs to pick up O2 d. V/Q imbalance= ventilation in the alveoli does not match the amount of perfusion e. If pt has normal perfusion but lack of ventilation= low V/Q ratio= shunt i. atelectasis, there is a decrease in air that reaches alveoli while there is a normal perfusion to that region ii. COPD iii. Asthma iv. Pneumonia v. Pneumothorax f. High V/Q ratio (high ventilation and low perfusion) issue with perfusion i. PE ii. Sickle cell anemia iii. Blood loss= low hbg g. V/Q study i. Pt inhales isotope to see where it is dispersed in the lungs 2. Acid base balance a. Hydrochloric acid is high give sodium bicarb b. 3 elements produced when hydrochloric acid combines with sodium bicarb= salt, water, HCO2 3. Acute Respiratory Failure (ARF) types a. Type 1= Hypoxemic normocapnic i. Low O2 levels (hypoxemia) in the blood with normal CO2 levels (normocapnic)- main issue is lungs are struggling to get O2 in ii. Causes= pneumonia, pulmonary edema, ARDS, high altitude sickness iii. Sx’s= cyanosis, SOB, increases respiratory rate b. Type 2= Hypoxemic hypercapnic i. Low levels of O2 (hypoxemia) with elevated CO2 (hypercapnia) ii. Causes= anything that impairs ventilation like COPD, asthma, iii. Sx’s= HA, confusion, drowsiness, CO2 build up effects brain 4. First signs of hypoxia a. Confusion, agitation, anxiety, tachypnea b. Respiratory alkalosis 5. Later signs of hypoxia a. dyspnea, cyanosis b. respiratory acidosis 6. ARF what is it a. Serious condition where the lungs are affected by widespread organ dysfunction. It involves fluid buildup in the lungs and damage to the membranes that allow gas exchange. ARDS is categorized into three levels of severity—mild, moderate, and severe—based on how low the oxygen levels are in the blood. b. We know they are in ARDS when we give them O2 and their oxygen does not change, the o2 can not cross the aveoli because of the fluid build up in the way c. PaO2 (how much O2 is getting from your lungs to your blood) norm= 80-100 d. PaCO2 (how well the lungs are removing CO2 into your blood) norm= 45-35 e. HCO3= 22-26 f. Mild (200 mg Hg less than PaO2/FiO2 less than or equal to 300 mm Hg with positive end-respiratory airway pressure [PEEP] or constant positive airway pressure [CPAP] greater than or equal to 5 cm H2O) i. So O2 in blood to the amount of O2 being breathed in= (PaO2/FiO2) is b/w 200-300 mm Hg ii. Happens when we use PEEP of CPAP set at 5 cm H2O or more g. Moderate (PaO2/FiO2 ratio is b/w 100- 200 mm Hg with PEEP greater than or equal to 5 cm H2O) h. Severe (PaO2/FiO2 less than or equal to 100 mm Hg with PEEP greater than or equal to 5 cm H2O). 7. Causes of ARF/ARDS- need more review a. Direct injuries- pneumonia, aspiration- food or drink in lungs, pneumothorax, downing, PE b. After the initial pulmonary injury, such as aspiration, chemical mediators are released, which damage the alveolar-capillary membrane and trigger other changes associated with ARDS. This damage can cause interstitial (not intracellular) edema and decreased (not increased) surfactant production. c. Indirect injuries- sepsis which is number one, burns, multiple blood transfusions, pancreatitis, drug OD, d. Pneumonia- can lead into sepsis e. PE- diagnostic test is V/Q scan f. Status asthmaticus= severe and life-threatening exacerbation of asthma that doesn’t respond to standard treatment such as bronchodilators, corticosteroids, O2, i. Requires intubation and mechanical ventilation g. Air leak disorders like Pneumothorax, tension pneumothorax, barotrauma h. Chest radiography finding of left pneumothorax= shifting of the mediastinum to right bc air is pushing 8. Risk factors for ARF/ARDS a. Sepsis b. Aspiration of gastric contents c. Diffuse pneumonia d. trauma 9. ARF assessment/Sx’s a. Hypoxemia i. Intrapulmonary shunting a main cause of hypoxemia where the result of blood passing through the lungs doesn’t partake in gas exchange, it’s like a traffic jam in the lungs ii. Low V/Q ratio iii. Examples are pneumonia and pulmonary edema b. Hypercapnia c. Acidosis i. Respiratory acidosis= low pH, high PaCO2 d. Depends of precipitating event and severity of the phase 10. Early vs later symptoms or ARF a. The early signs and symptoms of ARDS include i. dyspnea (difficulty breathing), ii. non-productive cough iii. restlessness, iv. clear chest X-ray (CXR) v. respiratory alkalosis (a decrease in blood carbon dioxide levels). b. significant changes in ARF i. CXR shows infiltration ii. respiratory acidosis (an increase in blood carbon dioxide levels) iii. Retractions, iv. accessory muscle use, v. pallor or cyanosis 11. ARF diagnosis a. ABG b. CBC- determine if the cause is from an infection c. Refractory hypoxemia= condition where a patient has low oxygen levels in the blood that do not improve despite receiving supplemental oxygen. This indicates a severe impairment in the lungs' ability to oxygenate blood, often seen in ARF, damage to the lung's structures leads to ineffective gas exchange, making it difficult for oxygen to enter the bloodstream, which can result in refractory hypoxemia. d. Chest x-ray i. “whiteout” on chest film= white on x-ray of lungs are not normal ii. White spots on x-ray of lungs can be severe pulmonary edema, pleural effusion, and atelectasis (collapse of lung) iii. Shows bilateral infiltration of lungs which is a classic sign of ARF e. Ventilation f. O2 therapy i. Positive end-expiratory pressure (PEEP) 1. Positive end-expiratory pressure (PEEP) is a mode of mechanical ventilation that keeps the airways open at the end of expiration (helps ensure that the remaining alveoli are filled with air when the pt exhales), preventing lung collapse and improving oxygenation. While PEEP itself is not a diagnostic tool, it can help assess the severity of acute respiratory failure (ARF) by: improving O2, identify lung compliance, and differentiating types of ARF 2. We have a little internal PEEP of 5, this is the lowest setting PEEP on vent 3. Positive and negative effects 4. Positive effects= improves oxygenation, reduce atelectasis, decrease work of breathing by keeping the airway open 5. Negative effects= decrease CO by reducing venous return to heart, barotrauma- subcutaneous emphysema(air trapped under the skin) is sign- see in puffy eyes and face, increased intrathoracic pressure 6. Treat low CO caused by PEEP= give fluids and positive inotropes, decrease PEEP 7. Symptoms of O2 toxicity= substernal chest pain that increases with deep breathing, increasing CO2, sore throat and eye and ear discomfort ii. Extracorporeal (ECMO) and intracorneal gas exchange 1. Extracorporeal gas exchange is used in cases of severe acute respiratory failure (ARF) when conventional ventilation methods are inadequate. 2. If the alveoli are destroyed or heart is failing this is used a. This involves the removal of blood from the body, passing it through an artificial device (like an oxygenator), and then returning it to the body. 3. Intracorneal gas exchange- less common- This refers to gas exchange processes that occur within the body but may be enhanced through medical interventions. This can include techniques that improve the efficiency of lung function. g. Tissue perfusion 12. Nursing management for ARF a. Optimizing oxygenation and ventilation i. Positioning—Prone positioning- this expands the lungs- do as early as possible ii. Preventing desaturation iii. Promoting secretion clearance b. Assess LOC c. Turn pt every 2 hours d. Maintain IV fluids as ordered/ e. Providing comfort and emotional support f. Maintain surveillance for complications 13. Drugs for ARDS a. Relief of bronchospasm i. SABAs and LABAs: like albuterol, anything ending in ol b. Reduction of airway inflammation i. corticosteroids c. Reduction of pulmonary congestion- failure to reduce secretions will decease PaO2 i. Diuretics, Mucinex, humidification in vent to help loosen up secretions, free water in enteral nutrition and IV fluids makes secretions more loose d. Treatment of pulmonary infections i. antibiotics e. Reduction of severe anxiety, pain and agitation i. Benzos, opioids 14. Types of pneumonia a. Pneumonia is infection of lungs that causes inflammation, fluid accumulation, impaired gas exchange b. CAP- community acquired pneumonia i. Biggest prevention is vaccines, 65 and older every 5 years ii. Diagnostic tests to diagnose are CBC for WBCs, chest x-ray (shows infiltration), sputum culture- culture identifies organism sensitivity gives best antibiotic that will treat the culture- in the meantime give broad spectrum antibiotics c. HAP- hospital acquired d. VAP- ventilator associated i. Biggest risk factor is inadequate infection control like poor hand hygiene, inconsistent use of sterile techniques ii. Keep HOB 30-45 degrees to prevent aspiration 15. Medical management of ARDS a. Oxygenation- use pulse ox and ABGs to assess and adjust O2 therapy b. Ventilation i. Noninvasive vent= CPAP or BiPAP ii. Invasive= mechanical ventilation c. Pharmacology i. Antibiotics ii. Antivirals iii. Corticosteroids iv. Synthetic surfactant d. Acidosis i. Assess ABGs to identify is resp. or metabolic acidosis ii. Improve ventilation by using bronchodilators or mechanical ventilation to treat resp. acidosis iii. Bicarbonate therapy in severe acidosis e. Nutrition support- start ASAP i. Enteral (feeding tubes) or parenteral (IV) nutrition 16. Complications of ARD a. Encephalopathy- disease or dysfunction of brain resulting in altered mental status and cognitive impairment b. Cardiac dysrhythmias c. Venous thromboembolism- heparin, lovenox, STDs helps stimulate muscles to release protein C which is an antiplatelet d. GI bleeding- PPI, H2 blockers, stressors increases stomach acid 17. Nursing management of ARD a. Optimizing oxygenation and ventilation i. Positioning ii. Preventing desaturation iii. Promoting secretion clearance b. Providing comfort and emotional support c. Maintaining surveillance for complications d. Educating the patient and family 18. Primary nursing diagnosis for ARD a. Impaired gas exchange b. Ineffective airway clearance c. Ineffective breathing pattern d. Dysfunctional ventilator weaning response e. Alteration in nutrition f. Risk for imbalance fluid volume r/t sodium and water retention 19. NIPPV: Non Invasive Positive Pressure Ventilation- the pt is doing the work of breathing- a patient can be intubated and do the work of breathing= weaning trials a. Used in the treatment of patients with acute or chronic respiratory failure. b. Not used for pts who are hemodynamical unstable, decrease LOC, or excessive secretions- must intubate c. NIPPV may be used for patients who refuse ETT but still desire some palliative ventilator support. d. During NIPPV a mask is placed tightly over the patient’s nose or nose and mouth, and the patient breathes spontaneously while positive pressure is delivered. e. BiPAP: Bilevel positive airway pressure- different pressure set for inhalation and for exhalation- just covers nose f. CPAP: Continuous positive airway pressure- pressure set the same for both inhalation and exhalation- covers nose and mouth g. Pt can’t take anything PO- need oral care every 2 hrs h. Risk for aspiration increases because of the pressure going in 20. High flow nasal cannula a. Heated and humidified oxygen has several benefits compared to standard oxygen therapy. Standard oxygen therapy delivered through a nasal cannula or another device, such as a non-rebreather mask (NRBM), delivers cold (not warmed) and dry (not humidified) gas. This cold, dry gas can lead to airway inflammation, increase airway resistance, and possibly impair secretion clearance. b. One obvious benefit is that the high-flow nasal cannula can deliver very high flow rates of gas to match a patient's inspiratory flow demands. This is important as patients in acute respiratory failure can become extremely tachypneic, and their peak inspiratory flows (PIF), which may normally be 30 L/min - 60 L/min at rest, can reach upwards of 120 L/min in acute respiratory failure. c. Patients often prefer the use of HFNC to that of non-invasive continuous or bilevel positive pressure ventilation (CPAP or BPAP) because the tight-fitting mask can be uncomfortable for some patients. d. The O2 can dry up the secretions so make sure they are hydrated e. Oral care every 2 hrs, check skin under mask every 2 hrs 21. Airway management and mechanical ventilation a. The patient requires intubation if they- i. Have an airway obstruction ii. Lacks protective reflexes iii. Needs suctioning iv. Needs ventilation assistance b. What can you use to maintain airway patency? i. O2, suctioning, nasopharyngeal or oropharyngeal airways, ETT, bronchodilators c. What do you need in the patient’s room? i. Suction equipment, O2 supplies, types of airways, monitoring devices, emergency meds, ambu bag d. Used for absence of respiratory effort or when apnea is anticipated i. Do rapid sequence intubation- pt is tachypneic, resps are in the 40spt e. Complication with ventilator sign in pt i. Pt has asymmetrical chest expansion, drop in O2 stat, mental status change f. Assist with reposition and vent alarm goes off of low tidal volume, pt SOB, sudden drop in SpO2= disconnect pt from ventilator and do ambu bag and troubleshoot the ventilator, call resp. therapy g. High pressure alarms i. Going off because there is something interfering with the ventilator and the pt 1. Pt coughing, sections, condensation collecting up in the tubing h. Low pressure alarms i. Something is disconnected i. Oral airway may be used before intubation- can’t use for conscious pts j. Nasal trumpet used for conscious patient k. ET tube (ETT): control of airway i. Size of the tube based on patient size ii. Men 8-9 iii. Women 7.5-8 iv. Verify placement by auscultation, CO2 detector- see color change to purple if in lungs, look for bilat chest mvmnts v. Get chest x-ray for extra confirmation l. Complications of ETT i. Tracheoesophageal fistula ii. Cricoid abscess iii. Tracheal stenosis iv. Tube obstruction m. Nursing interventions for ETT tubes i. Ensure the ETT is secure ii. Assess lung sounds every 2 hours 22. Meds for Intubation a. Neuromuscular blocking agents: block acetylcholine i. Succinylcholine chloride “sux” ii. Pancuronium bromide iii. Vecuronium bromide iv. Atracurium 1. Can be administered by an RN under the direction of the PCP 2. Patient must be sedated prior to administration!!! Go on a date before you suck= Etomidate before Sux 3. Neostgmine (Prostigmine) is the reversal agent for neuromuscular blocking agents. b. Sedative agents: BP measurement every min during intubation i. Etomidate and fentanyl ii. Ketamine iii. Versed 23. After intubation resp. therapist gets ABG- puts art line in 24. Complications of mechanical ventilation a. Dysrhythmias b. Hypotension- intrathoracic pressure increase which collapses large chest vessels and decreases CO c. Ventilation malfunction d. Self-Extubation e. Anxiety f. Nosocomial pneumonia (HAP) g. VAP h. Aspiration i. Barotrauma (pneumothorax)- occurs with elevated PEEP and elevated tidal volume settings= symptom= asymmetrical chest expansion j. Decreased cardiac output- decrease venous return to heart 25. What is ECMO- ExtraCorponeal membrane oxygenation a. Basically takes over the lungs and does their job outside of the patients body b. Oxygenating blood via membrane oxygenator outside the patient’s body c. Cannulas bringing blood out of the jugular and returning oxygenated blood through femoral , can also exit and return blood in same cannula 26. Why do we use ECMO a. Severe resp. or cardiac failure i. Reverse condition ii. Bridge to device or transplant b. Respiratory i. Hypoxemic resp. failure is PF ratio less than 50 ii. Hypercapnic Resp. failure 1. If pt Ph less than 7.2 iii. Bridge to lung transplant c. ECMO is a form of life support, doesn’t fix underlying cause 27. Pre/Post test a. To measure PaCO2 in a hemodynamically stable pt is to measure their End-Tidal CO2 b. When assessing an intubated pt, the nurse notes normal breath sounds on the rt side of chest and absent breath sounds on left side. What is the problem? i. Right mainstem intubation= If the endotracheal tube is inadvertently advanced too far, it can enter the right mainstem bronchus, leading to ventilation of only the right lung. This would result in normal breath sounds on the right side while the left lung receives little to no air, causing absent or diminished breath sounds on the left. 28. What risk factors need to be considered when prepping a pt for a thoracentesis- needle in chest used for plural effusion a. Unstable hemodynamics b. Coagulation defects c. Uncooperative pt 29. HCO3 is the acid-base component that reflects kidney function a. Kidneys kick in to compensate for resp. distress which can lead to kidney issues- bicarb increase. But if bicarb is very low the means their kidneys just suck b. DKA= Kussmaul resp-breath deeper and faster to compensate for acidotic state to try to lowing the CO2

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