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 BS 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

Pulmonary edema Treatment Goal: O2 Mech. Vent 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 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 Potassium Fluids I&O 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

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 potassium-depleting 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 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 PaCO2 pH i h Hypocapnia 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 Silicosis 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: #2 Wheezing Dyspnea 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 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 Radiation Metastasis Radiation To shrink or reduce symptoms

Lung Cancer Nursing intervention Preventative measures 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 client with cancer of the lung is receiving chemotherapy. The nurse will monitor blood values especially: RBC WBC PT/PTT K+ & Cl- These 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: Fatigue Nausea Dehydration Skin ulceration

Question? A 40-year-old man has developed Stomatitis after chemotherapy treatment. He should be encouraged to: Eat hot, spicy foods Brush his teeth after each meal and at bedtime Rinse his mouth with commercial mouthwash after each meal 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: Bathe it the same as any other part of the body Apply moisturizing lotion to prevent dryness Wipe is with clear water and pat dry as needed only Treat as a stage 1 decubitus ulcer

Question? Cancer pain is best managed with the use of A patient-controlled analgesia pump Short-acting opioids administered around the clock Frequent administration of breakthrough medications 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 Physical dependence Drug tolerance Addiction 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 Etiology/Contributing factors 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 Ecchymosis Crepitus 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 Ineffective ventilation 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 Expiration: Inspiration: Dyspnea Anxious Tachypnea Tachycardia Paradoxical respiration Expiration: Flail bulges mediastium affected side Inspiration: Flail collapses unaffected side

Flail chest Treatment Decrease the work load of breathing Chest tubes? Oxygen Intubation Mech. Ventilation Chest tubes? Stabilize chest severe