Acute Respiratory Distress Syndrome (ARDS) Notes PDF

**UNIT 2 : ACUTE RESPIRATORY DISTRESS SYNDROME** - - - - ARDS-occurs when **lung swelling causes fluid to build up in the tiny elastic air sacs in the lungs** - 1. 2. 3. - - 1. 2. 3. - - - - - - - - - **CLINICAL DISORDERS COMMONLY ASSOCIATED...

**UNIT 2 : ACUTE RESPIRATORY DISTRESS SYNDROME** - - - - ARDS-occurs when **lung swelling causes fluid to build up in the tiny elastic air sacs in the lungs** - 1. 2. 3. - - 1. 2. 3. - - - - - - - - - **CLINICAL DISORDERS COMMONLY ASSOCIATED WITH ARDS** **A. Direct Lung Injury** 1\. Inhalation injuries 2\. Pneumonia 3\. Pulmonary contusion- is a lung parenchymal injury without lung or vascular lacerations. caused by trauma 4\. Radiation **B. Indirect Lung Injury** 1\. Sepsis 2\. Multisystem trauma 3\. Multiple transfusions- at risk for blood born conditioned: septicemia 4\. Pancreatitis- inflammatory mediators affect the lungs - **1. Exudative (acute) phase - 0- 1 day** -Type I alveolar cells are destroyed -Gas exchange is disrupted \- Capillary membranes leak -Protein-rich fluids fill alveoli, resulting in complicated inflow of O2 and outflow of CO2 -Hyaline membranes are formed (lung compliance(**ability of the lungs or alveoli to distend = ARDS** )vs elasticity (**ability to recoil to return to its resting state = COPD PT.** )) **ASSESSMENT FINDINGS:** 1\. CXR -pulmonary infiltrates 2\. Tachypnea and dyspnea 3\. Use accessory muscles, but lung sounds may be clear 4\. **PAWP** may be less than 18 mm Hg 5\. Change in LOC **2. Proliferative phase - 7- 21 days** -requires spontaneous mechanical ventilation -Type II alveolar cells are damaged -Surfactant ( **mixture of lipoprotein that coats the alveolar-capillary membrane, which reduces surface tension (**role: distention and recoil of the alveoli**) to prevent lung collapse**) production declines -Peak Inspiratory Pressure increases -Compliance declines -Further loss of alveolar function -Ventilation and perfusion mismatch MANAGEMENT: - - ASSESSESMENT 1\. CXR: infiltrates ( elevation of diaphragm) 2\. Refractory hypoxemia with hypercarbia despite hyperventilation 3\. Crackles 4\. PA and PAW pressure increases 5\. RA pressure increases ( due to the pulmonary edema in the pul. system which increases pressure and congestion in the right side of the heart hence right atrial pressure increases) 6\. Right sided HF develops 7\. Agitation due to hypoxemia **3. Fibrotic phase - 3-4 weeks** -Development of fibrotic tissue in ACM -Decreased lung compliance -Worsening pulmonary hypertension -Increased dead space ventilation ASSESSMENT FINDINGS 1\. Leukocytosis and fever 2\. Worsening infiltrates on CXR 3\. Worsening hypoxemia and hypercarbia 4\. Decreased tissue perfusion 5\. Inc HR and dec BP 6\. Lactic acidosis 7\. End-organ dysfunction **MECH VENT PT: WATCH OUT FOR HYPOTENSION** , DUE TO THE ENTRY OF AIR INTO , IT MAY FILL THE RIB CAGE AND COMPRESS THE ORGANS INSIDE THE CAGE INCLUDING THE HEART , DUE TO THE COMPRESSION IT WILL DECREASE THE PRELOAD , WHICH WILL NOW DECREASES BLOOD PRESSURE AND CARDIAC OUTPUT **1. Blood Gas study** Hypoxemia Pa02 below 60 mmHg Sa02 below 90% Respiratory alkalosis in early stages  **2. Chest x ray** NR: - - - - - **COLLABORATIVE MANAGEMENT** 1\. Mechanical ventilation 2\. Oxygenation 3\. Ventilation **LUNG VOLUME/ CAPACITY** INSPIRATORY RV - maximal volume that can be inhaled in inspiratory level TIDAL VOL. - ADULT NORMAL VOLUME : 500 refers to the total air during inhalation and exhalation FUNCTIONAL RESIDUAL VOLUME \- vol. in the lungs at end expiratory level - - ERV - maximum vol. that can be exhaled at end expiratory **Inspiratory Capacity (IC)**:\ The maximum volume of air that can be inhaled after a normal exhalation. It is the sum of the tidal volume and the inspiratory reserve volume.\ **IC = Tidal Volume (TV) + Inspiratory Reserve Volume (IRV)** **Expiratory Reserve Volume (ERV)**:\ The additional amount of air that can be exhaled forcibly after the end of a normal exhalation. It represents the extra air that can be pushed out of the lungs. **Residual Volume (RV)**:\ The volume of air remaining in the lungs after a maximal exhalation. This air cannot be expelled, ensuring that the lungs do not collapse and can continue gas exchange between breaths. **Vital Capacity (VC)**:\ The total volume of air that can be exhaled after a maximal inhalation. It is the sum of the inspiratory reserve volume, tidal volume, and expiratory reserve volume.\ **VC = IRV + TV + ERV** **Inspiratory Reserve Volume (IRV)**:\ The extra volume of air that can be inhaled with maximum effort after a normal inhalation. This represents the reserve capacity the lungs have during deep breathing. **Tidal Volume (TV)**:\ The volume of air that is inhaled or exhaled during a normal, relaxed breath. **Functional Residual Capacity (FRC)**:\ The volume of air remaining in the lungs at the end of a normal exhalation. It is the sum of the expiratory reserve volume and the residual volume.\ **FRC = ERV + RV** **Total Lung Capacity (TLC)**:\ The total volume of air the lungs can hold after a maximal inhalation. It is the sum of all lung volumes: tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume.\ **TLC = TV + IRV + ERV + RV**  VILI-acute lung injury that develops during mechanical ventilation **LUNG TOXICITY** **Complications:** 1\. CNS- vertigo, nausea , and convulsions 2\. Lungs- decreased surfactant. due to oxygen level toxicity 3\. Eyes- pupillary constrictions **NOTE :** Positive pressure increases intra pulmonary pressure which compresses superior and inferior vena cava ( great vessels ) which decreases preload of the heart hence decreasing the cardiac output making the pt. hypotensive **TREATMENT** **General principles:** 1\. Recognition & treatment of underlying medical and surgical d/o **(SEPSIS HAS THE HIGHEST RISK TO HAVE ARDS)** 2\. Minimize procedures and their ,complications **(increased frequency of suctioning leads to desaturation)** 3\. Prophylaxis: Thromboembolism **(compression stocking , enoxaparin subq z track method),** GI bleeding , aspiration , excessive sedation **(relaxation of the respiratory muscles)** , CVC infections. 4\. Prompt recognition of nosocomial infections. 5\. Provision of adequate nutrition. **USED OF MECHANICAL VENTILATORS:** **Ventilator-Induced Lung Injury (VILI)** Repeated alveolar distention- Recurrent alveolar collapse- PREVENT ALVEOLAR COLLAPSE If end-expiratory pressure is LOW =alveolar collapse **PEEP !!!** Improve oxygenation: Increase Mean Airway Pressure Inverse ratio ventilation\" (IRV) - to allow the lungs to adapt the increasing airway pressure Normal: Inspiration ( mas matagal na and inspiration than ex.) : Expiration ratio 1:1-1:2 OTHER THERAPIES 1\. Glucocorticoids(anti inflammatory - reduce the inflammatory effects of the pt. lungs) 2\. Other therapies Inhaled Nitric Oxide( dilator - transient oxygenation improvement) NURSING MANAGEMENT: **6 Ps of ARDS treatment** **1.Prevention** 1\. Prevent spread of pathogens 2\. Line care, Oral care \* 3\. Keep head of bed in proper position Note: VAP( ventilator associated pneumonia) \- 22.8% of patients with MV \- 80% of nosocomial pneumonias **2.Paralysis** Sedation: Propofol, Fentanyl, Midazolam (1st 24 - 48 hours) (-) : Neuromuscular weakness Increased ventilator time Increased length of stay **Remember**: Decrease 02 consumption **MANIFESTATIONS** a\. Minimizing fever - because it increases oxygen consumption b\. Activity level c\. Respiratory effort d\. Minimize suctioning - the higher frequency the higher risk for desaturation  **3.Positioning** Prone- **the heart is no longer laying against the posterior part of the lungs (improves air flow,hence improvement of lung sounds)** \- Implementation remains limited -Most effective when utilized early in the disorder \- EFFECTIVE WHEN :Pa02 rises 10 mm Hg within 30 mins **4 &5.Pump and Pipes** FLUID MANAGEMENT Reduce left atrial filling pressure: a\. Fluid restriction b\. Diuretics **Maintaining a normal or low left atrial filling pressure:** - - - - **6.VPEEP** **ACUTE RESPIRATORY FAILURE (ARF)-Rapid onset of respiratory impairment** A change in gas exchange (02 & CO2) Pa02 less than 60 mm Hg PaCO2 greater than 50 mm Hg pH less than or equal to 7.30 **LEADS TO:** - - - - **I. Impaired Ventilation** -SCI-due to weakness or paralysis of the respiratory muscles. \- Phrenic Nerve **( controls the movement of the diaphragm )** damage \- Neuromuscular blockade \- Guillain-Barre Syndrome- ascending paralysis which affects lung movements \- CNS depression - drug overdose ( specifically downers- narcotics and sedatives ) \- Respiratory muscle fatigue- due to ARDS **II.Impaired gas exchange** -Pulmonary edema -ARDS -Aspiration pneumonia- destroys capillary membranes **III.Airway obstruction** -Aspiration of foreign body -Thoracic tumors -Asthma \- Bronchitis \- Pneumonia **IV- Ventilation Perfusion Abnormalities** **-Pulmonary embolism -**a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream. **-Emphysema-** the air sacs in the lungs (alveoli) are damaged. (SOB) **Signs and symptoms of ARF** **1. Hypoxemia** **2. Restlessness** **3. Tachypnea, Dyspnea** **4. Tachycardia-** due to sympathetic response **5. Confusion-** due to decreased cerebral blood flow and oxygenation **6.Diaphoresis, anxiety, irritability** **7. Hypercarbia** **8. Somnolence (late)** **9. Cyanosis (late)** **10. Loss of Consciousness (late)** **11. Pallor or cyanosis of skin** **12. Use of accessory muscles of respiration** **13**. Abnormal breath sounds- **crackles**( asthma) and **wheezes** (pulmonary edema or secretions ) **DIAGNOSTIC TESTS:** **1. ABG** Pa02 less 60 mm Hg PaCO2 more than 50 mm Hg pH less than 7.30 **MANAGEMENT**: **IMPROVE OXYGENATION & VENTILATION** 1\. Supplemental 02 (Pa02 greater than 60 mm Hg) 2\. Bronchodilators, Mucolytics (acetyl), CPT, Positioning ( beta 2 agonist- check the heart rate because the drug can cause tachycardia) 3\. Suction as indicated (never on a routine schedule) - lead to desaturated, hyper oxygenate first before doing suctioning ( not beyond 10 secs). **WATCH OUT FOR:** a\. Desaturation b\. Cardiac arrhythmias, respiratory distress -Bronchospasm \- Increased RR c\. Increased BP or ICP d\. Anxiety, pain or change in mental status **REDUCE ANXIETY:** 1\. Give brief explanation of activities and approaches being done to relieve ARF 2\. Presence of nurse during anxious periods 3\. Diaphragmatic breathing 4\. Mild doses of Anxiolytics (lorazepam, diazepam) **PREVENT AND MANAGE COMPLICATIONS** **1. Pulmonary aspiration** \- Continuous gastric aspiration -Ensure proper inflation of ET cuff **2. GI bleeding** -Check gastric aspirate for presence of occult blood every 4-8 hours \- Anti-ulcer agents **3. Barotrauma** \- Avoid unnecessary increases in airway pressure -Assess signs of pneumothorax( desaturation, decreased respiratory rate, decreased air entry via auscultation) **4. Volutrauma** \- Prevent alveolar damage from excessive TV **ACUTE CORONARY SYNDROME** - -  **THE HIGHER THE CLASS THE HIGHER SEVERITY** **RISK FACTORS:** - - - - - **PATHOPHYSIOLOGY** 1\. Plaque rupture or erosion 2\. Dynamic obstruction 3\. Progressive mechanical obstruction 4\. UA secondary to increased oxygen demand and/or supply **Precipitating factors:** 1\. Vigorous physical exercise 2\. Emotional stress 3.medical or surgical illness **note : circadian rhythm** **CLINICAL PRESENTATION:** **1. History & PE** Chest pain levine sign-a clenched fist held over the chest to describe ischemic chest pain **Location:** Substernal region; epigastrium **Radiates to:** Neck, Left shoulder,Left arm **Note: Silent heart attacks** **MISTAKEN IMPRESSION!!** - - **PHYSICAL FINDINGS:** 1\. Anxious and restless 2\. Pallor, perspiration, coolness of extremities 3\. Tachycardia & HPN 4\. Bradycardia & hypotension 5\. Apical pulse may be difficult to palpate 6\. 3rd and 4th heart sounds 7\. Decreased intensity of 1st heart sound 8\. Split S2 9\. Carotid pulse: decreased volume **2. Electrocardiogram** 30% - 50% NSTEMI patients ST segment depression T wave inversion Transient ST segment elevation  **3. Cardiac Biomarkers** Elevated CK MB and troponin - - - Increased risk for death or recurrent MI Troponin elevation=Mortality LABORATORY FINDINGS 1\. Cardiac imaging 2\. Non specific indices of tissue necrosis and inflammation Onset to 3-1 days WBC: 12,000-15,000/uL. 2 D Echocardiography Decision: Reperfusion therapy? Fibrinolysis or PCI STRESS TESTING 1\. Clinical history 2\. ECG 3\. Cardiac markers 4\. Stress testing **TREATMENT** 1\. Medical treatment Bed rest Continuous ECG monitoring v Ambulation = C/I: Discomfort; ECG Changes Biomarkers **ANTI- ISCHEMIA** **1. Nitrates** SL 3 doses (5 min apart) Buccal spray (0.3 - 0.6 mg) IV: 5-10 ug/min Topical and oral nitrates **CONTRAINDICATION**: Hypotension Sildenafil (previous 24-48 hours) **2. Beta Adrenergic blockers \[olol\]** **3. ACE inhibitors \[pril\]** **4. HMG COA reductase inhibitors \[statin\]** **ANTI- THROMBOTIC** **1. Aspirin (ASA)** **Initial dose: 325 mg/ dose** **Lower: 75- 162 mg/ dose** **2. Clopidogrel (P2Y12 / ADP inhibitor)** **Loading: 300/ 600 mg** **75 mg/ dose (PRIOR to PCI)** **1. Unfractioned Heparin (UFH)** **2. Low Molecular Weight Heparin** **(LMWH) Enoxaparin** **3. Fondaparinux (Indirect Factor Xa inhibitor)** **4. Bivilirudin (Direct thrombin inhibitor)** **INVASIVE VS CONSERVATIVE STRATEGY** STRATEGY: 1\. Anti ischemic 2\. Anti-thrombotic 3\. Coronary angiography- a type of radiography of blood vessels following injection of a die; carried out within 48 hours from admission 4\. Coronary revascularization- follows CA, which includes PCI or CABG **Unstable Angina/ NSTEMI ANGIOGRAPHY** **Based on angiography:** Approx. 5%: stenosis of the Left Main Coronary artery 15%: 3 vessel CAD 30%: 2 vessel CAD  - - - LOW RISK PATIENTS: Strategy: 1\. Anti- ischemic 2\. Anti- thrombotic 3\. \"watchful waiting\"-the pt. Will be monitored if there will be monitored for the ff: - - **EMERGENCY DEPT** 1\. Oxygen- due to interrupted coronary blood flow because of the myocardial ischemia that causes an imbalance of myocardial oxygen demand and supply - 2\. Aspirin- to manage suspected ST-elevation MI, Inhibits Cox 1 platelets followed by the reduction of thromboxane A2, which is a local vasoconstrictor 3\. Nitroglycerine- decreases myocardial oxygen demand by lowering pre load and increases o2 supply by dilating the vessels 4\. Morphine (2-4 mg IV q 5 min)- to manage the discomfort and chest pain, But WOF for reduced cardiac output and hypotension this occurs due to venous pooling because Morphine reduces sympathetically mediated arteriolar and venous constriction 5\. Beta-blockers(olol)- reduce myocardial oxygen demand and ischemia; this is given provided that the HR is greater than 60 bpm because it can cause bradycardia, as well as the systolic bp, maintaining more than 100 mmHg.  SAVE THE ISCHEMIC PENUMBRA - - CABG- FOR PT. WHO HAS ACS - - INDICATION 1\. Has failed medical management 2\. More than 2 disease coronary vessels with significant blockage 3\. Not a candidate for PCI 4\. Has failed PCI attempt with ongoing chest discomfort, indicating that there is a blockage or poor perfusion in the myocardium ADVANTAGES: 1\. Patients with C/I to fibrinolysis- e.g., pt. Who has bleeding tendencies 2\. More effective than fibrinolysis 3\. Better short term and long term outcomes DISADVANTAGES: 1\. Expensive-1-2 million pesos 2\. Applicability is limited by its availability FIBRINOLYSIS - FOR ACS patients - - - AGENTS: **MOA: t**o promote the conversion of plasminogen to plasmin, which subsequently under fibrin thrombi 1\. Tissue Plasminogen Activator (PA) 2\. Streptokinase (Streptase) \[to prevent hypotension, give it with slow controlled infusion within 30-60 mins. \] after which, give \+ Heparin IV bolus 5,000 units \+ Infusion of 1,000 units/hr 3\. Tenecteplase (TNK) 4\. Reteplase (Retavase) CONTRAINDICATIONS of FIBRO.: 1\. CVA OR H. OF CEREBROVASCULAR HEMORRHAGE; Non- Non-hemorrhagic stroke 2\. Severe uncontrolled hypertension at risk for bleeding 3\. Suspicion of aortic dissection 4\. Active internal bleeding 5\. Surgery within the past 2 months **HOSPITAL PHASE MANAGEMENT** COMPLICATIONS 1\. Ventricular dysfunction- HF with ejection fraction of less than 40% meaning there is a poor pumping of the heart 2\. Hypovolemia- due to diuretics, reduced fluid intake, vomiting, which leads to hypotension and vascular collapse 3\. Cardiogenic shock- inability of the heart to pump adequately 4\. Right ventricular infarction (1/3) 5\. Arrhythmia: VT, VF **NOTE!!** 1\. Deaths due to VF (Ist 24 hours) 2\. Delay: onset of pain=pt. decision - NURSING INTERVENTIONS: 1\. Relieve pain and others signs and symptoms of ischemia 2\. Improve respiratory function 3\. Promote adequate tissue perfusion 4\. Reduce anxiety 5\. Monitor and manage potential complications 6\. Promote home and community based care **ICU NURSE** 1\. Activity- to reduce cardiac workload Bed rest for 12 hours Note: -may assume Upright position \- Dangle feet \- Sit in a chair with supervision -ROM of the legs to prevent thrombophlebitis and blood clot formation -Sex: 4-6 weeks after the hospital. Or tolerate an exercise without having chest discomfort 2\. Diet NO or clear liquids (1st 4-12 hours) 3\. Bowel management Bedside commode High bulk diet- to prevent constipation Stool softeners/ Laxative 4\. Sedation Diazepam 5mg Oxazepam 15-30 mg Lorazepam 0.5-2 mg LONG TERM MANAGEMENT Risk Factor Modification 1\. Smoking cessation 2\. Achieve optimal weight 3\. Daily exercise and appropriate diet 4\. BP control 5\. Hyperglycemic control 6\. Lipid control **SHOCK** **a condition in which the cardiovascular system fails to perfuse the tissues adequately resulting in widespread impairment of cellular metabolism** **Classifications** **1. Cardiogenic** **2. Hypovolemic** **3. Obstructive** **4. Distributive** - - - **Causes:** 1\. Myocardial ischemia & infarction 2\. Arrhythmias 3\. Heart Failure 4\. Cardiac tamponade-Compression of the heart due to fluid accumulation within the pericardium 5\. Cardiomyopathy **Hypovolemic Shock** A. Hemorrhagic Surgery Trauma GI bleeding Ruptured aneurysm B. Non- hemorrhagic Vomiting; Diarrhea Burns Severe dehydration **Obstructive Shock** Pulmonary embolism Aortic dissection **Anaphylactic Shock** Contrast media Drug reactions BT reactions Food allergies Insect bites or stings Snake bites **Septic Shock** Cause: Widespread infection Release of chemical mediators Vasodilation **Neurogenic Shock** Damage or dysfunction of the sympathetic nervous system Trauma Anesthesia Spinal shock  **COLLABORATIVE CARE** **General Measures** A. Oxygen and Ventilation B. Fluid Resuscitation C. Drug Therapy D. Nutritional Therapy **A. Correction of the Underlying Cause:** 1\. Cardiogenic \- Remove coronary obstruction \- Restore blood flow 2\. Hypovolemic \- Identify source and stop bleeding \- Correct fluid shunting or third spacing with electrolyte management 3\. Anaphylactic \- Intubate \- Treat allergic reaction/ Epinephrine 4\. Septic \- Antibiotic therapy 5\. Neurogenic \- Severing of the cord may be irreversible \- Intubation **B. Improve Oxygenation** 1\. Assess airway and intubate if necessary 2\. Administer oxygen at 100% or as necessary until Pa02 is adequate (\>60-70mm Hg) **C. Restore adequate Tissue Perfusion** 1\. Administer fluid volume expanders (PNSS; PLRS) 2\. Blood transfusion (hypovolemic) 3\. Vasoactive drug therapy **DRUGS** 1\. Dobutamine 2\. Dopamine 3\. Norepinephrine 4\. Arginine-Vasopressin (ADH)