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Lower Respiratory Disorders Continued Pulmonary edema - Aspiration Pulmonary edema • Rapid shift of fluid from the plasma to pulmonary interstitial tissue and alveoli • Causes impaired gas exchange Pulmonary edema • d/t – left ventricular failure – Backed up blood in the pulmonary vein – h pressure in pulmonary vascular system – Fluids “leak” into interstitial space & alveoli Pulmonary edema Etiology / Contributing factors • Left ventricular failure • Fluid overload – IV’s • Drug OD Pulmonary edema Clinical Manifestations • Dyspnea – Sudden – Orthopnea – Cyanotic (central) – “air hunger” – Tachypnea • Cough – Copious sputum – Frothy – Blood tinged Pulmonary edema Clinical Manifestations • Pulse – Tachycardia – Bounding • BS – Crackles • Fine course • Engorged neck & hand veins Pulmonary edema Clinical Manifestations • Anxiety • Confusion • Stupor Pulmonary edema Diagnostic exam • Auscultation – Crackles • X-ray • V/S – Tachycardia – Tachypnea • Pulse oximetry – i • ABG’s – PaO2 • i Pulmonary edema Treatment • Goal: – Remove fluid – h oxygenation • O2 – Mask • Non-rebreather • Mech. Vent – PEEP Pulmonary edema • Diuretics – Lasix • Digitalis / Digoxin lanoxin Bronchodilators – Aminophylline • Morphine – i peripheral resistance – i pressure in pulmonary capillaries – i leakage – i anxiety Pulmonary edema • A. B. C. D. E. Which of the following electrolytes must be closely monitored in a patient on Lasix diuretic therapy? Chloride Hydrogen Magnesium Potassium Sodium Pulmonary edema • What nursing actions must be performed before administering digitalis? – This is not multiple choice – you should know this one cold! • What do you do if the apical pulse is <60? Pulmonary edema Diagnosis: • Impaired Gas Exchange: the fluid –filled alveoli decreases the exchange of gases Out come: • the client will demonstrate improved gas exchange, as evidenced by rising PO2 to 55 or 60 mm Hg, Oxygen saturation above 90%, normaralizing pH, decreasing anxiety and dyspnea, and fewer crackles Pulmonary edema Nursing management • Diet – Sodium • Low – Potassium • High – Fluids • Decreased / restricted • I&O • Weights – Q day Pulmonary edema Nursing management • Position to promote circulation – HOB h – Dangle legs Pulmonary edema Nursing management • Provide psychological support • Monitor meds Acute Respiratory Failure Definition • Sudden & life-threatening • i gas exchange “It exists when the exchange of O2 for CO2 in the lungs cannot keep us with the rate of O2 consumption & CO2 production.” • Ventilation & Perfusion are impaired Acute Respiratory Failure ABG’s • PaO2 – < 50 mmHg • PaCO2 – > 50 mmHg • Arterial pH – < 7.35 Acute Respiratory Failure Causes of ARF • i respiratory drive – TBI, MS, Sedatives, hypothyroidism • Dysfunction of the chest wall – Nerve, spinal cord, neuromuscular junction disorders • Dysfunctional Lung Parenchyma Acute Respiratory Failure S&S • Early – – – – – Restlessness Fatigue H/A Dyspnea Respirations • Air hunger – Pulse • h – BP • h Acute Respiratory Failure S&S • Progresses – – – – Confusion Central cyanosis Diaphoresis Resp. arrest Acute Respiratory Failure Nursing management • Assist with intubation & maintain mechanical ventilation • Assess respiratory status – – – – LOC ABG’s SpO2 VS Acute Respiratory Failure Nursing management • Implement strategies to prevent complications – – – – TCDB Oral care Skin care ROM • Address problems that led to ARF Acute Respiratory Distress Syndrome • AKA – ARDS – Adult Respiratory distress syndrome Acute Respiratory Distress Syndrome • • • • ARDS is acute, Severe injury to most or all of both lungs. ARDS is not a specific disease; ARDS can be confused with congestive heart failure • IT is respiratory failure that occurs as a result of massive trauma to the lungs Acute Respiratory Distress Syndrome • Characterized by – – – – – • • sudden and progressive pulmonary edema increasing bilateral infiltrates on chest x-ray Hypoxemia reduced lung compliance Not due to left side heart failure Occurs as a result of injury to alveolar capillary membrane (D/T: aspiration, drug OD, smoke, infection, shock, trauma, sepsis*) Acute Respiratory Distress Syndrome • • • • • Injury Inflammatory response release chemical (histamine etc.) which cause injury to the alveolar capillary membrane Leakage of fluid into the alveolar interstitial space and alt. Capillary beds Protein, blood cells and fluid enter alveoli Acute Respiratory Distress Syndrome • Decrease in surfactant • Alveoli collapse (atelectasis) and fibrotic changes • Lungs become stiff, less compliant, very hard to inspire • Decrease in gas exchange /shunted • Hypoxia • Atelectasis and edema worsen • Lungs may hemorrhage Acute Respiratory Distress Syndrome • Etiology/Contributing factors – – – – – Infection Trauma Narcotic OD, Inhalation of irritants Aspiration Acute Respiratory Distress Syndrome • Clinical manifestations – Rapid onset of severe dyspnea • • • • – with in 12-48 hours Intercostal and suprasternal retractions Increased resp rate Crackles Hypoxemia that does not respond to O2 • • • Confusion anxiety Restlessness, apprehension Cyanosis Acute Respiratory Distress Syndrome – ABG’s • PaO2 – < 70mmHg • PaCO2 – > 35 • HCO3 – Normal – < 22 • pH – low • Analysis – Resp. and met. Acidosis Acute Respiratory Distress Syndrome • Diagnostic exams/procedures – X-ray • appears to be white due to excessive fluid in the lungs Acute Respiratory Distress Syndrome • Treatment – O2 Intubation and mechanical vent. • – Maintain PaO2 at > 60mm Hg PEEP • • • • – Improves oxygenation Increases functional residual capacity Reverse alveolar collapse Use a lower FiO2 Systemic hypotension • Fluid leakage Acute Respiratory Distress Syndrome – – – – Pulmonary vasodilators Surfactant replacement Corticosteroids Sedatives • due to anxiety and ventilator – Diuretics – Circulatory support • Adequate fluid volume – May limit fluids – Nutritional – Neuromuscular blockers / paralytic drugs Acute Respiratory Distress Syndrome • Nursing intervention – – Rest Change position • monitor O2 sat in different positions – – • High fowlers Prone Complications – – High death rate (50-60%) No one recovers 100% Pulmonary Hypertension • Pathophysiology – Pulmonary arteries narrow • – Vasoconstriction Increased Pulmonary BP • – (>30 mmHg) How do you measure pulmonary BP? • Only can be measured during right side heart catheterization Pulmonary Hypertension • Pathophysiology – If increase in BP – Right ventricle has to work harder – Right ventricle hypertrophy • enlargement and dilation – Right ventricle fails • Precursor to Cor Pulmonale Pulmonary Hypertension • Etiology/Contributing factors – Primary: • • • • • – Rare Female > Male Age 20-40 years hereditary tendency usually die within 5 years of diagnosis Secondary: • Existing cardiac or pulmonary disease – – Mitral valve disease COPD Pulmonary Hypertension • Clinical manifestations of – Pulmonary hypertension without right sided heart failure • • • • (Not clinically evident until late in progression) Dyspnea and fatigue that worsens over time Cyanosis and Tachypnea Crackles and decrease breath sounds Pulmonary Hypertension • Clinical manifestations of… – Right sided heart failure • • • • • • Peripheral edema Ascites Distended neck veins Liver engorgement Crackles Heart murmur Pulmonary Hypertension • Diagnostic exams/procedures – ABG’s: • PaO2 – – • Decreased Hypoxemia PaCO2 – – Increased Hypercapnia Pulmonary Hypertension • Diagnostic exams – ECG • Shows right ventricular hypertrophy – Cardiac catheterization • Right sided heart catheterization only way to measure pulmonary pressure – X-ray – Pulmonary function test Pulmonary Hypertension • Treatment – – – Oxygen therapy Vasodilators (in some people) Anticoagulants – • – – Warfarin (Coumadin) Diuretic to decrease blood volume Heart/lung transplant – Really there is no cure – death within 2-3 years of diagnosis unless transplant Pulmonary Hypertension • A 66-year-old client takes a potassiumdepleting diuretic. Foods that will help to keep the client’s potassium level within normal limits include – – – – – – Bananas Oranges Cantaloupe fish Spinach whole-grain cereals Pulmonary Heart Disease • Pathophysiology – Right ventricular failure d/t increased pulmonary pressure – Pulmonary artery vasoconstriction – Right ventricle has to work harder – Right ventricle fails Pulmonary Heart Disease – Right ventricle does not empty normally – Backward buildup – Increase in Right atrial and systemic venous blood volume – Jugular neck veins distend – Peripheral edema – Angina from right ventricle ischemia Pulmonary Heart Disease • Clinical Manifestations (right vent. failure) – Edema • Feet • Legs – Distended neck veins – Enlarged palpable liver – Pleural effusion – Ascites – Heart murmur Pulmonary Heart Disease • Medical treatment – Improve ventilation • Treat lung disease • Treat heart disease – Lung disease • O2 • Chest physiotherapy • Bronchial hygiene • Intubation – Heart disease • Bed rest • Na restriction • Diuretic • Digitalis Pulmonary Heart Disease • Nursing management – Monitor ventilators – Monitor heart and lungs • • • • O2 Na Restriction diet Diuretics Stop smoking Pulmonary Emboli Pathophysiology • Emboli: – foreign object that travels through the blood stream • • • • blood clot Air Fat Thrombus (thrombi – pl) – A stationary clot Pulmonary Emboli • Emboli travels into a pulmonary artery causing obstruction – Ventilation/perfusion mismatch • Ventilation – Yes • Perfusion – no – CO2 • h • respiratory acidosis Pulmonary Emboli Etiology/Contributing factors • Most PE originate in deep veins of the lower extremities • Deep Vein Thrombosis – DVT Pulmonary Emboli S&S of DVT • Positive Homan’s sign – Pain w/ passive dorsiflexion • calf tenderness & swelling • Unilateral • Warm distal extremities • Skin discoloration • Superficial vein distention Pulmonary Emboli • A. B. C. Does a person with DVT have pedal pulses? Yes No I think I’ll just wait for Mrs. Keele to reveal the answer! Pulmonary Emboli Risk Factors for DVT • Surgery w/ general anesthesia • Fx of the lower extremities • Heart failure • Bed rest / paralyses • Obesity • Amniotic Fluid Embolism and air embolism Pulmonary Emboli Prevention of DVT • Leg exercises • X sitting cross legged • Drink fluids • Anticoagulant therapy Pulmonary Emboli Complications of Anticoagulant therapy • Wear shoes • Use an electric razor • Use a soft toothbrush • Easy bruising • Nose bleeds • Bleeding that does not stop Pulmonary Emboli • Blood in urine • Blood in sputum – black stools • Changes in menstrual flow • Avoid aspirin • Lab work on time • If lactating an infant – P baby for S&S too • Elderly – Close monitoring Pulmonary Emboli Treatment of DVT • naturally dissolves – 7-10 days • Bed rest – strict! • Anticoagulant therapy – Heparin • Route? – – – – IV Sub q never IM Warfarin Sodium/ Coumadin Labs? – • PTT/PT Pulmonary Emboli • O2 • Thrombolytic agents – Streptokinase – Urokinase Pulmonary Emboli Clinical manifestations of PE • Sudden onset – Dyspnea – Tachypnea – sharp chest pain – Cough – Hemoptysis • Gasping for breath & anxious • Death with in one hour! • Venous return is – i – Jugular venous distention Pulmonary Emboli • ABG’s: – PaO2 • i – PaCO2 • h • Hypocapnia – pH • i • Respiratory Acidosis Pulmonary Emboli Dx exams/procedures • Lung scan • Pulmonary angiogram • ABG’s • CT* • MRI* – * only show if large Pulmonary Emboli Nursing intervention • Assess resp distress / function • ID patients at risk – ambulation – range of motion – sequential/ted hose • Assess for Homan’s sign • P heart failure • Educate about – anticoagulant therapy – Prevention – S&S Pulmonary Emboli • • • • • • • • • • Avoid leaving IV catheters in for long time If SOB, HOB h O2 as prescribed Pulse Oximetry Opioids for sever pain Anticoagulation per MD – Monitor for complications Enc. to verbalize fear Nebulizer tx I.S. Chest physiotherapy Pulmonary Emboli Complications • Right ventricle unable to push blood into the occluded artery • Weak contractions • i cardiac output • Hypotension • Increase BP within the pulmonary circulation • Right ventricular failure • Cor Pulmonale Sarcoidosis • Pathophysiology – A granulomatous disease that affects many body systems – A tumor like mass or nodule of granulation tissue • due to chronic inflammatory process – Hypersensitivity response to one or more agents Sarcoidosis • Clinical manifestations – – – – – – – – Insidious onset – lack of prominent S&S Dyspnea Cough Hemoptysis Congestion Anorexia Fatigue Weight loss Sarcoidosis • Assessment & Dx – X-ray – CT scan – Biopsy – ABG’s • Varied – Normal – Hypoxemia – Hypercapnia Sarcoidosis • Medical management – Remission without specific treatment – Corticosteroids Pneumoconioses • • • • • – – – – – – – – Occupational lung disease Pathophysiology Non neoplastic alteration of the lung secondary to exposure to inorganic dust Silicosis silica dust mining, quarrying and tunneling operators Asbestosis Asbestos Dust no cure Coal workers pneumoconiosis Black Lung disease Lung Cancer Pathophysiology • Carcinogen binds to the DNA and changes it • Abnormal growth • Usually develops on the wall of the bronchial tree FYI • Lung Cancer is the number one cancer killer in the US Lung Cancer Etiology/Contributing factors • #1 – Tobacco Smoke (85%) – Second hand smoke • Carcinogens – Asbestos – Uranium – Arsenic – Nickel – Iron oxide – Radon – Coal dust Lung Cancer Clinical manifestations: early • Insidiously and asymptomatic until late stages FYI – 70% of lung CA have metastasized by the time of diagnosis Lung Cancer S&S: Early • Objective symptoms – #1: • Cough – #2 • Repeated respiratory tract infection – Wheezing – Dyspnea Lung Cancer S&S: Late • Hemoptysis • Chest pain • Pleural friction rub • Pleural effusion • Finger Clubbing • Wt loss • Anemia • Anorexia Lung Cancer • A. B. C. D. E. F. When Lung cells mutate due to cancer, they frequently produce and secrete what endocrine hormone? ACTH T3 (thyroxin) FSH ADH Insulin Growth hormone Lung Cancer • An increase secretion of ADH due to lung cancer is diagnosed as what disorder? – No hints this time, can you name it? – Turn to your neighbor and show them how smart you are! Lung Cancer Dx exams/procedures • X-ray • CT scan • Biopsy via Bronchoscopy Lung Cancer Treatment • Removal of Ca tumor • Chemotherapy – • Metastasis Radiation – To shrink or reduce symptoms Lung Cancer • Nursing intervention – – – – – – Dyspnea Anorexia Pain control Fatigue Grief Hospice • Preventative measures – #1 • Stop smoking Lung Cancer Clients receiving chemotherapy • Enc client to eat soft, non-irritating foods high in protein • Watch for S/E of chemotherapy and radiation • Administer antiemetics and anti-diarrheals • Provide good skin care • Reverse isolation – Leukopenia – neutrophil • Stomatitis – inflammation of the mucous membranes of the mouth Lung Cancer • A. B. C. D. E. A client with cancer of the lung is receiving chemotherapy. The nurse will monitor blood values especially: RBC WBC PT/PTT K+ & ClThese drugs depress the bone marrow, inhibiting the production of blood cells, and a serious decrease in WBC’s increases susceptibility to infection Chemotherapy Question? The most likely side effect of chemotherapy is: A. Fatigue B. Nausea C. Dehydration D. Skin ulceration Question? A 40-year-old man has developed Stomatitis after chemotherapy treatment. He should be encouraged to: A. Eat hot, spicy foods B. Brush his teeth after each meal and at bedtime C. Rinse his mouth with commercial mouthwash after each meal D. Drink plenty of orange juice Question? A 62-year-old client is receiving radiation treatments for lung cancer. The field for radiation therapy is clearly outlined with purple ink. The nurse would treat this field as follows: a. Bathe it the same as any other part of the body b. Apply moisturizing lotion to prevent dryness c. Wipe is with clear water and pat dry as needed only d. Treat as a stage 1 decubitus ulcer Question? Cancer pain is best managed with the use of A. A patient-controlled analgesia pump B. Short-acting opioids administered around the clock C. Frequent administration of breakthrough medications D. Long-acting opioids administered around the clock Question? A client taking opiods for cancer pain begins to require more medication to provide the same amount of analgesia. This is known as A. Physical dependence B. Drug tolerance C. Addiction D. Equianalgesia Lung Cancer Preventative measures • Stop smoking Lung Cancer • Complications – – – – – Pleural effusion Tumor obstructs Superior vena Cava Ectopic hormone Production • mimics the bodies own hormones • ADH (anti diuretic hormone) = SIADH (syndrome of inappropriate ADH) No urine output • ACTH (Adrenocorticotropic hormone) = Cushing syndrome Atelectasis & Pneumonia Metastasis (brain, bone, lung, liver, lymphnodes) Rib fractures • Pathophysiology – usually 4th – 9th rib – If 1-3 rib high mortality rate • Etiology/Contributing factors – – – – Blunt vs. Penetrating Spleen and liver damage Trauma Uncontrolled coughing Rib fractures • Clinical manifestations – Pain • • Severe aggravated by – Movement – Breathing – coughing – – – – Ecchymosis Crepitus Swelling Deformity Rib fractures • Diagnostic exams/procedures – – – – X-ray ECG O2 SATs ABG’s Rib fractures • Treatment – Detect and treat other injuries – Do Not use elastic rib belts • (decrease breathing) – Control pain • • • so TCDB decrease complications If needed an intercostal nerve block – Ribs generally heal in about 6 weeks – Ice packs Flail chest • Pathophysiology – When multiple ribs are fractures, structural support of the chest is impaired – Ribs are fractures at 2 or more sites Flail chest – Paradoxical respiration • Normal – I – Chest expands • Normal – E – Chest shrinks • Flail chest – I – Area of flail chest collapses • Flail chest – E – Area of flail Chest bulges – Ineffective ventilation • Hypoxia Flail chest • S&S – – – – – Dyspnea Anxious Tachypnea Tachycardia Paradoxical respiration • Expiration: – – • Flail bulges mediastium » affected side Inspiration: – – Flail collapses mediastium » unaffected side Flail chest • Treatment – Decrease the work load of breathing • • • Oxygen Intubation Mech. Ventilation – Chest tubes? – Stabilize chest • severe