Patho Exam 2 - Respiratory Disorders
Bronchoscopy with Biopsy
-Anesthesia or conscious sedation -Put tube down into lung -Get sample of tumor
Asthma triggers
-Allergens -Cold Air -Viral infections -Smoke -Occupational -ASA/ NSAIDS -GERD -Anxiety -Identify what triggers their asthma symptoms -What are their allergens -Cold air can trigger asthma symptoms -Respiratory infection +Asthma = bad!!! -Smoking/second-hand smoke -Occupational: dust, smoke, fumes (wear mask!!!!) -Asprin or NSAID drugs can trigger some people -GERD: GI problems/acid reflux can irritate the upper airways -Anxiety can trigger more bronchial spasms
Anticholinergics
*Impritroprium (Atrovent®) -Anticholinergic inhalers: blocks acetylcholine (parasympathetic: constricts lungs) blocks bronchoconstriction
Corticosteroids
*Inhaled *Oral or IV -Corticosteroids: manage the inflammation (inhaler delivers corticosteroid into the lungs... drugs that inhibit cortisol) -Oral/IV has more side effects. -Inhaled works locally. -Bronchodilators: manage bronchoconstriction
Leukotriene Inhibitors
*Montelukast (Singulair®) -Leukotrienes: late-phase allergic chemicals that can cause broncho spasms ; inhibitors help control symptoms
Beta 2 agnoists
*Short-acting (Albuterol) *Long-acting (Salmeterol) -Beta 2 receptors: in lungs, respond to sympathetic, open up airways -Short-acting B2 (Albuterol): works fast, but doesn't act that long! Used to treat someone with acute symptoms... rescue inhaler! Quickly relieves symptoms -Long acting B2 (Salmeterol): takes longer to start working, but lasts 8-12 hours. Maintenance inhaler. Not designed to quickly relieve symptoms... it is preventative!!
Lung Cancer Risk Factors
-80% are associated with cigarette smoking -Asbestos another risk factor -Genetic predisposition -Radon -Asbestos: mineral that was used in insulation and industrial uses, really fine threads that if you inhale, it goes in your lungs and never goes away. It sits in there and irritates things and causes mutations -Radon: an odorless, colorless gas that comes out of the ground; radioactive; can occur in people's houses; periodically have your basement tested for radon
Emphysema
-A serious disease that destroys lung tissue and causes breathing difficulties. -Destruction of the terminal bronchioles with air trapping -Decreased surface area for gas exchange airways collapse when exhaling -Air stuck in lungs... dead, stale, deoxygenated air stuck in lungs -Barrell-chest... full of trapped air -Alveoli dissingrate; less surface area for gas exchange
Pleural effusion
-Accumulation of fluid in the pleural space -Effusion: accumulation of fluid -Pleura: membrane around the lungs -Visceral pleura: directly around lungs -In between pleura, some pleural fluid to lubricate it, but should barely be able to see it -If the fluid builds up, it can start to push the lungs in and affect its function
Mechanisms of Hypercapnia
-Airflow Obstruction: *COPD, Asthma, CF -Decreased Respiratory Drive: *Drug Overdose, Brainstem Injury, Brain Injury, SCI -Thoracic Deformities: *Flail Chest -Neuromuscular Disorders: *Guillain-Barre Syndrome, Myasthenia Gravis, ALS -Reasons patients carbon dioxide levels go up: *COPD, asthma, cystic fibrosis *Neurological problem... respiratory drive can be inhibited. *Too much opioid suppresses respiratory center in brain stem: you cant breathe and die *Spinal cord injury can inhibit your ability to breathe. *Paralysis of respiratory muscles
COPD Nursing Management
-Assessment -Maintaining Oxygenation -Med Administration -Hydration -Pulmonary Rehab -Patient Education -Pursed Lip Breathing -Energy Conservation -Medication/ O2 teaching -Psychosocial Support -Advanced Directives -Assessing their symptoms, listen to lungs, vitals, oxygen stats Goal: improve their oxygenation -Oxygen supplements, meds -Pulmonary rehab gradually improve their ability to exercise in monitored conditions -Teach patient pursed lip breathing... do this when breathing out and air will come out more effectively -Energy conservation... teach them how to structure their day -Teach them about their medicines and oxygen... oxygen safety (don't smoke around it!!! Can cause fire) Don't turn dial all the way up... that's dangerous!!! There's a prescribed level!!!! -Psychosocial support: help them cope with their illness -Advanced directives: some people no longer want to be intubated... they would rather pass away
Lung Cancer
-Average age of diagnosis 71 -5 year survival for men 6-14% -5 year survival for women 7-18% -DEADLIEST cancer in the US! -Leading cause of cancer death for both genders. -Highest mortality.
Asthma: treatment
-Avoidance of Triggers -Pneumovax and Annual Flu Vaccine -Desensitization -Medications
Pulmonary emoblism (PE)
-Blockage of pulmonary artery or main branches by thrombi, fat or air. -Pathophysiology: *Clot migrates from deep veins in the legs *Obstruction of pulmonary vessels causes a mismatch of ventilation and perfusion *Vasoconstriction in the area increases pulmonary artery pressure and right ventricular pressure -Blockage of one of the pulmonary arteries or branches by something that's not supposed to be there -Thrombi: clots (usually caused by this!) -Blood comes back from right side of heart from venous system, right side pumps the blood out to pulmonary artery, which delivers it to lungs to be oxygenated and remove CO2. Oxygenated blood comes back to left side of the heart to be pushed out to the body. -If you have a clot that comes from your nervous system (ex. Your leg) if that clot breaks off, it will travel until it reaches a branch in the pulmonary artery system where it gets stuck, and then blocks a segment of lung area from getting that blood flow -Deep vein thrombosis: in leg -Mismatch between ventilation and perfusion. All alveoli should have a 1:1 match between air flow and blood flow around that capillary bed so that there's blood to absorb the oxygen and get rid of CO2 -Wherever the area is blocked, there's no blood going to that area. Theres no way for that part of the blood to oxygenate that area. -Ventilation mismatch results in hypoexmia: or low blood oxygen -Creates back pressure on the right side of the heart
Incentive spirometer
-Breath in to make it move!!!! -Breathe in and feel lungs expand... ball moves up device... much more effective to do a slow deep breath... (keep the right ball in the marked section)
Lung cancer: diagnosis
-Bronchoscopy -Biopsy -CT/MRI -PET scan -Biopsy to confirm the type of cancer. -Bronchoscopy: put tube down into lung and get a biopsy directly off the tumor -If tumor not accessible, a surgical biopsy may be needed. -Then, do CT/MRI to see how spread the disease is. Look for metastasis -PET scanning combines nuclear medicine and imaging to cause areas of high metabolism to light up (cancer is highly metabolic)
PE Diagnosis
-CT Angiogram -V/Q Scan. -D-Dimer. -Venous Doppler. -Pulmonary Angiography -Test of choice: CT Angiogram (contrast dye to get an adequate picture; advanced CT) -If a person cant have contrast dye due to liver function or allergy, then they do V/Q scan. -Ventilation perfusion (V/Q): inhale and take pictures to look for matchup: do all the areas that light up when they breathe light up from the blood? If not, there's a mismatch. -D-dimer: blood test that measures clotting activity in the body. D-dimer will be elevated if there's a blood clot. -Problem: lots of things can elevate the D-dimer such as a bruise, surgery, -If D-dimer is negative, we can pretty safely rule out clot. -If positive, there MIGHT be a clot, but we don't know. They need to do imaging to look for an actual clot. -PE will probably come from legs... doppler legs to see if theres more clot in their legs. -Any question about the diagnosis, they can do angiography (invasive test: inject pulmonary artery and take pictures... rare bc its risky/dangerous)
Lung cancer: screening issues
-CXR not effective -CT New Recommendations -Difficult to screen for -Ex. Colonoscopy effective screening test for colon cancer; can find the cancer at an early stage and treat it -Chest X Rays don't work for screening for lung cancer. Once the tumor shows up on the x ray, it's already too late. -Heavy smokers can have CT scannings
Pleural effusion: diagnosis
-CXR or CT -Thoracentesis -Chest X ray should show the effusion... if they want more detail about location/extent/malignancy, do a CT -If not sure what's going on, tap the effusion and get sample of the fluid! -Thoracentesis: thorax aspiration of the fluid
Exudate (cloudy fluid)
-Caused by capillary damage -Infection -Malignancy -Empyema -Exudate: cloudy fluid; caused by malignancies or infections... pneumonia can cause pus that starts to leak into pleural space (pus: dead white blood cells, bacteria, and debri) -Empyema: big collection of pus -Cancers tend to damage the vascular structures and cause fluid leakage
Transudate (serous fluid)
-Caused by high fluid pressures -Heart Failure -Low serum albumin -Transudate: clear fluid; heart failure can cause this... if the heart is damaged and not pumping effectively, fluid backs up into the lung, can cause capillary leakage into pleura -also, low serum albumin causes problems with fluid shifts -(albumin: large molecules that pull fluid with it) -If albumin level drops, for ex. A nutritional issue or disease, fluid leaks out of vessels and into interstitial spaces including pleural spaces
Signs of Impending Respiratory Failure
-Changes in Mental Status -Patient requires Tripod Position to Breathe -Inability to Speak in Complete Sentences -Continued Hypoxia despite administration of high flow O2 -Decrease in Respiratory Rate and Effort Despite continued hypoxia -Careful assessment is important. Watch their mental status. Lethargic, some change in their mentation, confused, agitated... is this a problem with gas exchange? Are they obtaining CO2? Are they getting oxygen? -Tripod position: respiratory distress (Sitting forward, using every ounce of energy to breathe) -So short of breath that they cant complete sentences... very severe!!!!! Respiratory failure sign -Oxygen level remains low despite getting oxygen... problematic!!!! -Really ready to crash when theyre getting exhausted and respiratory rate slows down... need tube bc theyre about to crash
COPD
-Chronic Obstructive Pulmonary Disease -Airflow obstruction -Not fully reversible -Risk Factors: *Tobacco smoke *Occupational -Permanent damage; degree of airway obstruction that is no longer reversible -Tobacco smoke is leading etiology to COPD!!!! -occupational is some risk -People who have COPD usually has emphysema and chronic bronchitis... usually 1-2 of them -COPD is usually an umbrella term for the 3 of them
Emphysema: pathophysiology
-Cigarette smoke and other irritants stimulate release proteases which are enzymes that damage lung tissue -Individuals with lower levels of α1-antitrypsin are at higher risk -Results in hyperinflation because airways collapse on expiration and destroyed alveoli result in loss of surface area for gas exchange -Barrel Chest -"Pink Puffers": accessory muscle use and lack of cyanosis -Proteases: enzymes that break down tissue -Alpha 1 antitrypsin: clear out proteases -Alpha 1 antitrypsin deficiency: very severe COPD at young ages bc damage happens very rapidly -Airway collapse on expiration, destroyed alveoli, barrel chest -Emphysema: Pink Puffers... they work very hard to breathe, use a lot of accessory muscles, pink in color, breathing very labored
Asthma: diagnosis
-Clinical History and Exam -Spirometry -Methacholine Challenge -How long have you had asthma? How do you manage it? What are your symptoms? What triggers it? How severe is it? What meds/adjustments help? -If new diagnosis, spirometry testing... measure aspects of air movement and lung volume -If diagnosis is unclear, methacholine is a cholinergic agent (if bronchial spasms, then test is positive. They reacted to the methacholine)
Atelectasis continued
-Clinical Manifestation: *Fever, dyspnea, diminished breath sounds, crackles, decreased SpO2 -Diagnosis: *Clinical history and exam *CXR -Prevention/Treatment: *Early mobilization, Incentive spirometer, cough/deep breathe, early mobilization, hydration -Treatment: *Remove obstruction, bronchodilator -Fever for 24 hours after surgery, alveoli are stuck together and pop open when breath in which cause crackles -Are they post-op, do they have a mucous plug? -Chest X Ray -Incentive spirometer: they breath in and the device moves up and shows how much air theyre bringing into their lungs, sticky mucous = more likely it will plug up, so drink a lot to keep mucous thin! -Bronchoscope aspirate the obstruction
Pulmonary Hypertension continued
-Clinical Manifestations: *Dyspnea, fatigue, dizziness, right sided heart failure -Diagnosis: *Echocardiogram -Treatment: *Supplemental oxygen *Sildenafil (Viagra®) *Lung transplant -Straining right side of heart and making it hard to get blood to the lungs... start to fail (causes fluid to back up to the body -> edema) -Echocardiogram: ultrasound of the heart -Sildenafil (Viagra): acts as a vasodilator... relaxes the vessels.
Atelectasis
-Collapsing of alveoli in a segment or multiple lung segments -Etiology: *Compression of large or small bronchus *Obstruction *Tumor *Mucous Plug -Post-operative: Anesthesia and diaphragmatic dysfunction lead to alveolar collapse -Atelectasis: some of your alveoli start to collapse; air sacs collapsing -Caused by a blockage or surgical complication -Postoperative patients tend to get atelectasis because alveolar get sticky and tend to collapse; diaphragm weaker; patient not moving a lot
COPD Complications
-Cor Pulmonale -Weight Loss -Exacerbations -Chronic Hypoxia -Hypercapnia -Depression/Anxiety -Respiratory Failure -4th leading cause of death -Cor Pulmonale: right-sided heart failure caused by chronic lung disease (puts back pressure on right side of the heart) Right side of the heart receives blood back from the body and pushes it to the lungs; damage leads to blood backflowing to heart -Using all calories in order to breathe... difficulty eating with breathing problems... weight loss -Exacerbation: flare-up of their symptoms -Hypercapnia: chronically elevated levels of CO2 -Panic-inducing feeling... not getting enough air; major impact on life -Respiratory failure: their respiratory situation is so severe they can no longer do gas exchange... leads to ventilator
Acute Respiratory Distress Syndrome (ARDS)
-Damage to Alveolar-Capillary Membrane Results in Increased Permeability -Alveoli Fill with Fluid -Development of Intrapulmonary Shunt -Loss of Surfactant Results in Alveolar Collapse and Decreased Lung Compliance -Accumulation of Hyaline membrane -Necrotic Cells, Protein and Fibrin -Further Impairs Gas Exchange -High Mortality Rate (up to 50%) -Often due to MODS -Tube may be put in, or ventilator, then fix underlying reason for resp. failure -ARDS: something damages the membrane, fluid starts to leak into the alveoli and fill (damage: direct lung injury or caused by abnormal systematic inflammation) .. -Results in intrapulmonary stunt: mismatch is so severe that deoxygenated blood is coming back into the left side of the heart... not going to be able to fix this hypoxemia without a ventilator -After the alveoli fill with fluid, the damage to the membrane inhibits surfactant (which is needed to keep alveoli from sticking together) -Now you have fluid in the lungs that become stiff and hard to open -Lungs very resistant to opening up now -Eventually, there can be an accumulation of debri and scarring that can lead to permanent lung damage -Often die to multi-organ dysfunction syndrome (MODS)
Pneumothorax: diagnosis and treatment
-Diagnosis: CXR -Treatment: *Small pneumothorax may be observed and allowed to re-absorb *Chest Tube *Supplemental Oxygen *Analgesics -Diagnosed by chest xray -May go away on its own -Chest tube can evacuate the air -We may provide oxygen and pain medicine
Diagnosis of ARDS
-Diffuse Bilateral Infiltrates on CXR -No Evidence of Heart Failure -ARDS: we cant get their oxygen level up to a reasonable level even with high flow oxygen/ventilator *****
Etiology of ARDS
-Direct Lung Injury: *Aspiration *Near Drowning *Severe bacterial or viral pneumonia *Chemical Inhalation -Systemic Inflammation *Sepsis *Trauma *Pancreatitis *Shock -ARDS is triggered by direct injury to the lungs or systematic inflammation -Throws up and aspirates on vomit can damage the alveoli membrane -Inflamamtion can get out of control and cause damage. -Septic: systematic infection that's triggering an inflammatory reaction causes lung damage -Pancreatitis: inflammation of pancreas; associated with severe inflammation that damages lungs -Trauma and shock can induce inflammation that can damage the lung
Pleural effusion: clinical manifestations
-Dyspnea, Diminished breath sounds, dullness on percussion -s/s of infection or cancer if related to these diagnoses -As fluid accumulates, it can press against the lungs and cause shortness of breath -Fluid goes down by gravity, less breath sounds at the bottom of the lungs -Bigger effusion = further up the decreased breath sounds will go -Dull = fluid
PE Clinical Manifestations
-Dyspnea, tachycardia, tachypnea, hypoxia. -Anxiety -Pleuritic chest pain. -Cough and Hemoptysis. -Hypotension, Shock. -Pulmonary Hypertension -Sudden collapse and death -Issues with oxygenation. Short of breath. Heart rate goes up. Breathing faster. O2 stats low. -Lack of oxygen may leave you anxious. -Pleuritic chest pain: pain that occurs from taking a deep breath or coughing (anything that stretches the lungs) -Hemoptysis: coughing up blood -Severe large PE, if you block a main segment of an artery, you're blocking blood from returning to the left side of the heart, which causes cardiac output to bottom out, blood pressure bottom up, and die.
Pulmonary hypertension
-Elevated pressures in the pulmonary circulation -Pulmonary Artery Hypertension (PAH) -Mean pulmonary artery pressure > 25 mm Hg at rest and > 30 mm Hg with exercise -Pathophysiology: *Fibrosis of vessels and vasoconstriction raises pressures -Etiology: *Idiopathic *Chronic Lung Disease *Recurrent PEs -High pressures in the pulmonary arteries coming from right side of the heart -Normal pulmonary artery pressure: 25-30 depending on activity -Reasons why the pressures might get high: if you have damage on vessels and they become narrowed, pressure can raise. Or chronic lung disease -Why does it happen? Idiopathic (don't know why) chronic lung disease or recurrent PE
Pneumothorax
-Entry of air into the pleural space. -Loss of negative pressure causes lung to collapse -Should not have air in pleural space -If you lose contact between the two layers, the lung collapses. -Pneumothorax can occur from acute damage or spontaneously
Virchow's triad
-Factors predisposing to thrombophlebitis: -Venous Stasis: Immobility -Endothelial Damage: Venous Disease -Hypercoagulability *Estrogen *Genetic coagulopathies *Cancer *Pregnancy 1. Elderly, Immobility, CHF, Atrial Fib, Bedrest, CVA, Varicose Veins, Pregnancy, Orthopedic Surgery. 2. IVs, Trauma, Previous Clot, Leg fractures. 3. Smoking, Dehydration, Malignancy, OCPs, HRT, Coagulation defects, Sepsis. -Hypercoagulability: factors that make the blood more likely to clot -Muscle contraction and valves need to move blood back to the heart... if not moving for a long time, the blood just sits there in the veins and will start to clot. (ex. People on long airplane rides can get these from sitting for so long without moving) -Immobility is a risk factor. -Endothelial damage: clots start at this point -Estrogen: promotes clot formation; women who are pregnant or just delivered a baby are at high risk!! Birth control is high risk of blood clots -Genetic disorders can make people more prone to blood clots... may need to be on some type of anticoagulant -Presence of cancer can stimulate the body's clotting mechanism
Cystic fibrosis: pathophysiology
-Genetic Disorder: Autosomal Recessive -Involves exocrine glands of respiratory, GI, and reproductive tracts -Epithelial membrane impermeable to chloride ion *Results in increased NaCl in sweat *Lowers water content of respiratory and pancreatic secretions -Exocrine function: release of digestive enzymes into the intestines -Pancreas clogs up and fails to release digestive enzymes... causes malabosorption problem
ILD: diagnosis
-History of exposures -Decreased lung volumes and diffusion on PFTs -CT -Were they exposed to any toxins, dust, smoke, etc.? -Were they prescribed any toxic drugs? -COPD and asthma: low FEV1, but inspiratory volumes aren't low; low FVC -Restrictive lung disease/ISL: PVTs are low; all volumes are low because its hard to fill the lungs in the first place -Damage will show up on CT scan
PE Treatment
-Hospitalization. -Heparin Drip. -O2 to maintain sats. -Morphine for pain. -Monitor ABG's, coags, V/S, EKG, Cardiopulmonary status. -Possible IVC filter. -PE is an indication to hospitalize patient because it can be life-threatening -Heparin: inhibits clotting system; anticoagulant; prevents new clots from forming or present ones from worsening -Thrombolytics: goes in and dissolves the clot -Look at coagulation labs... we need to anti-coagulate them enough to prevent clots, but not too much that they bleed -Look at vital signs and look at EKG to see if its straining the right side of the heart -IVC filter: inferior vena cava... if concern that more clot may embolism, they put a filter in inferior vena cava to prevent clot
Chronic bronchitis: pathophysiology
-Hypersecretion of mucus with hypertrophy of mucus glands in response to irritants like cigarette smoke -Plugging of airway lumens, inflammation, and fibrosis of bronchioles -Increased incidence of respiratory infections -Hypoxemia stimulates polycythemia and vasoconstriction -"Blue Bloaters": Cyanosis and edema from right sided heart failure -Lots of mucous with chronic bronchitis in response to the irritants!! Mucous clogs up and cause damage to the lining of the bronchial -Growth medium for bacteria... reoccurring bacterial infections -Hypoxemia: more difficult to oxygenate -Pulmonary vessels constrict and strain right side of the heart... right-sided heart failure... fluids back up to the rest of the body -Hypoexmia... cyanotic... r side of heart damage; fluid back up and cause edema..., BLUE BOATERS -High levels of red blood cells: polycthemia
Inhaled Corticosteroids
-Indicated for chronic management -Decreased adverse effects -Most effective -Must be used consistently -Not for rescue -Rinse mouth after use -Orally affects the whole body! -Inhaled decreases adverse effects and works locally -Rinse mouth after: it suppresses immune function... residue that sits in the mouth can lead diminished immune function...yeast can grow in the mouth
Chronic bronchitis
-Inflammation of bronchi persisting over a long time -Type of chronic obstructive pulmonary disease (COPD) -Productive cough for 3 months in 2 consecutive years -Sputum
Chest tube
-Inserted in pleural space -Purpose: Evacuate air or fluid -Assessment: *Vitals *SpO2 *Pulmonary *COCA *Pain -Trend their vital signs -Look at heart rate, temp, respiratory rate, oxygen saturation, pulmonary assessment, breath sounds, if there's drainage COCA (color, odor, consistency, amount), pain
Thoracentesis
-MD inserts needle into pleural space -Purpose: Diagnostic or Therapeutic -Positioning: Sitting up -Nursing Responsibilities: *Consent *Maintain Sterility *Instruct Patient *Post-procedure Assessment -Want them sitting/leaning over bedside table -Invasive tests, need to sign an informed consent!!! Explain procedure -Sterile conditions required! -Instruct patient to hold still while putting needle in -Assess patient afterward; did their symptoms improve? Did they develop a complication such a bleeding or collapsed lung?
Spirometry
-Measures of Obstructive Disease: *Forced Vital Capacity (FVC) *Forced Expiratory Volume in 1 second (FEV1) *Peak Expiratory Flow Rate -Interpretation Dependent On: *Age *Gender *Ethnicity *Height -Measure how much air you can blow out in 1 second (with asthma, it's lower) -Peak expiratory flow rate - home test that person can use to see how their asthma is doing -Decreased force vital capacity
Inhaled corticosteroids are mainstay of treatment for persistent asthma
-Mild, intermittent asthma or solely exercise-induced asthma, may solely use B2 agnostics -More reoccurring asthma: inhaled corticosteroids
ILD: Clinical manifestations
-Non-productive cough, exertional dyspnea -Fine bibasilar crackles -A dry cough, shortness of breath especially on exertion, fine crackles at the bases
Atelectasis: pathophysiology
-Obstructive: *When bronchus is obstructed air is absorbed and the alveolus collapses *Alveoli may also fill with fluid -Post-operative: *Decreased diaphragmatic excursion *Hypoventilation *Decreased surfactant activity -When bronchus is obstructed, everything else will collapse -Hypoventilation: not breathing enough; short, shallow breaths
Hypoexmic
-Oxygenation failure.. poor oxygenation -Arterial oxygen level of 60 mm Hg or less on 60% oxygen -(Normal level: 80-100)
Oxygenation Requirements
-Patent Airway -Adequate Breathing -Effective Gas Exchange -Adequate Tissue Perfusion -Sufficient level of hemoglobin -All cells need oxygen -If oxygen is cut off, brain cells will start dying in 4 minutes. -All of these things need to be present for oxygenation to occur. -Need a method for air to get to lungs (patent airway) -Lung disorders, nervous system disorders (brainstem damage), musculoskeletal damage, neuromuscular diseases that paralyze breathing muscles, can all affect breathing -Alveolar gases must pass through to participate in gas exchange -In order for oxygen to get out of the body, perfusion needs to occur through cardiovascular -Hemoglobin carries oxygen to the cells. -Everything must coordinate together
Interstitial Lung Disease (ILD)
-Pathophysiology: *Stiff non-compliant lungs (Restrictive lung disease) *Normal airways but lung is difficult to expand *Fibrosis of alveolar membrane -Etiology: *Occupational Inhalants *Drug Toxicity *Amiodarone, Methotrexate *Autoimmune *Idiopathic -Obstructive lung disease: lots of air trapped... hard to get oxygenated air in -Interstitial lung disease: lungs are stiff and resistant to filling... difficult to expand; airways are resistant to filling in the first place -Asthma: lungs are hyperinflated -If the membrane becomes fibroytic or scarred, gas exchange becomes difficult because its hard to move past the scarring -Occupational inhalants: chemicals, dust, smoke, (ex. Black lung disease - coal miners without respiratory protection... inhale coal dust for decades and scar their lungs) -Drugs can induce pulmonary fibrosis. -Amiodarone: a drug for cardiac rhythm disorders -Methotrexate: chemotherapy agent that can be used for autoimmune diseases (need to see if it damages the lungs) -Idiopathic: we don't know why it happens! (im an idiot, Idk why it happens...)
Lung cancer: local involvement in lung
-Persistent Cough (early sign) -Dyspnea, airway obstruction, hemoptysis -Pain is a late symptom -By the time the person develops symptoms, the disease is already intensive -Persistent cough... but smokers cough anyway, so they don't realize it's serious and related to cancer -Can obstruct bronchial tubes, which can lead to shortness of breath and tissue damage, which can bleed and cause coughing up blood = hemoptysis -Pain is a LATE symptom... cancer has metastasized already.
Tension Pneumothorax
-Pneumothorax when air enters the pleural space and can't escape -As air accumulates, pressure builds in thorax and begins to compress mediastinal structures -Clinical Manifestations: *Same as pneumothorax with tracheal deviation, hypotension, muffled heart sounds, shock and death if not resolved -Treatment: *Emergent chest tube insertion or needle *Thoracostomy -Associated problem that can occur is a tension pneymothrorax -Allowing air to come in but trapping it... cannot vent. -Buildup of air causes pressure that pushes everything over. -Eventually will push on heart, aorta, vena cava, and affect cardiac output -Tracheal deviation: pushes trachea toward unaffected side -BP will drop, cardiac output will drop, heart sounds will sound distant -If we don't fix the problem, person will go into shock and die -Life-threating emergency!!! Put in chest tube or needle into pleural space to allow air to vent
Peak flow meter
-Portable Measure -Best of 3 Attempts -Compare to Baseline -Self-Management -Green Zone: *80% or above *Maintain present therapy -Yellow Zone: *60-80% *Use rescue inhaler *If not improved call provider -Red Zone: *Below 60% *Use rescue inhaler *Seek emergent care -Patient can use this to gauge where their asthma is -Portable device that they blow into... shows peak expiratory flow -Do it 3 times. Take best from 3 times. -Find a baseline... normal peak flow for that patient. Compare what you got today to what their norm is. Ex. Baseline: 500 mL peak flow.... Today: 450 mL peak flow..... 450/500 = 90% -As long as they are 80% or better, they are green zone! That's good! -320/500 = 64% That's yellow zone... not good. Use rescue inhaler, wait a few minutes, and retest. If not back in green zone, call provider. -240/500 = 48% That's red zone... use rescue inhaler and get to E.D. bad shape!!!! Dangerous! -Green: 80% and above -Yellow: 60-80% -Red: Below 60%
Spontaneous Pneumothorax
-Primary: *Congenital defect results in bleb *Most commonly occurs in tall, thin, white men *Risk factors include family history and smoking -Secondary: *Emphysema -Defect in pleural lining -Congenital: you were born with it -Typically, tall, thin, white man!!!!!! -Once had once, it can reoccur!!! -Secondary: severe emphysema can cause damage to the lung which can cause this to occur
Respiratory failure
-Problem severe enough in gas exchange that the body can no longer compensate for it -One or the other, or both (Hypercapnic or hypoxemic) -when we cant get their oxygen up even with supplemental oxygen
ILD: treatment
-Remove offending agent -Corticosteroids -Supplemental Oxygen -Lung Transplant -Remove offending agent such as a medication or exposure to prevent further damage -Corticosteroids: to suppress inflammation causing the scarring, especially if its autoimmune
Asthma
-Reversible Airway Obstruction -Pathophysiology: *Airway inflammation and bronchoconstriction *Release of cytokines and mediators *Airway hyper-reactivity *Mucous cell hyperplasia *IgE mediated response to common allergens -Asthma results in reversible airway obstruction. -Inflammation and bronchoconstriction!!!! -Linings of airways are inflamed and irritated -Bronchoconstriction: smooth muscle in bronchial tubes tighten up; airways tighten up -Allergies can trigger this -Airways become hyper-reactive: any other irritants such as smoke or cold air can cause lung to spasm more -Mucous cell become hyperplasia: or hyperactive
Lung cancer: Paraneoplastic Syndromes
-SIADH (Ectopic ADH) -Cushing Syndrome (Ectopic ACTH) -Eaton-Lambert Syndrome *Autoimmune attack on neuromuscular junction -Paraneoplastic syndromes: manifestations of the cancer caused by enzymes that the tumor secretes -ADH: antidieurtic hormone; makes you hold water and dilute your plasma -(high level of ADH: Syndrome of Inappropriate Antidiuretic Hormone SIADH) -Cushing Syndome: too much cortisol! Releasing ACTH -Eaton-Lambert Syndrome: cancer stimulates antibodies that can affect neuromuscular junction/muscle weakness
Status Asthmaticus
-Severe, acute asthma -Life Threatening -History of Intubation -Silent Chest -Respiratory Effort -Initial ABGs: PO2↓ PCO2↓ pH↑ -Late ABGs: PO2↓ PCO2↑ pH↓ -Ever have a breathing tube put down them?Intubation? -At risk to have to get breathing tube again -No sounds is worst than wheezing... not moving any air at all. Wheezing means there is air moving. -Sometimes wheezing means theyre getting better bc air is starting to move through. -Initially, oxygenation drops and they are severely SOB, labored breathing, hyperventilating, blowing off lots of CO2, bc theyre hyperventilating bc theyre trying to get more air in, Ph is going up -As things get worst, they're getting exhausted and can't maintain the effort anymore... they're acidic and will crash
Lung Cancer Cell Type
-Small Cell -Non-Small Cell: *Squamous Cell Carcinoma *Adenocarcinoma -Small cell: more aggressive, harder to treat -Non-small cell: squamous or adenocarcinoma -Squamous cell carcinoma: comes from squamous epithelial cells that line your lung -Adenocarcinoma: mucosa cells
COPD: Treatment
-Smoking Cessation -Pneumovax and annual flu vaccine -Anticholinergic Inhalers: *Short Acting: Ipratropium (Atrovent®) *Long Acting: Tiotropium (Spiriva®) -Corticosteroids: *Inhaled for maintenance *Oral or IV for acute exacerbations -Antibiotics for Exacerbations -Supplemental O2 -Medicare criteria SpO2 < 88%, PO2 < 55mm Hg > 15 hours/day increased survival for hypoxemia -Caution with high flow oxygen -Stop whatever is damaging the lungs! -Smoking cessation prevents disease from accelerating -Inhalers for asthma can be used for COPD -Long-acting: maintenance -Normal: 80-100 on blood gas SpO2 -We are driven to take a breath based on our CO2 levels -COPD has chronically elevated CO2 levels -Too much O2 will knock out the respiratory drive
Pneumothorax: etiology
-Spontaneous: Ruptured bleb -Trauma: Penetrating or rib fracture -Iatrogenic *Thoracentesis *Insertion of central line or pacemaker *High pressure mechanical ventilation -Ruptured bleb: weak spot that gives away (spontaneous) -Iatrogenic: caused by healthcare (WE did it to them) caused by medical intervention --Thoracentesis: pushed needle in too far --Central line or pacemaker threaded into vein; incision made and devices sewed up, you can nip the pleura and cause this --High pressure ventilation can cause lung to rupture
Assessing Oxygenation
-Subjective -Vitals -SpO2 or ABG -Color -LOC -Respiratory -Cardiac -Periphery -Always start with assessment. Tells where the person is and what to do from there. -Always start with subjective. How do you feel? Any issues with oxygenation? Any difficulties breathing, shortness of breath, chest pain? COLDSPA! Dyspnea, when did it start, how severe 0-10, is it getting better/worse? What improves it? Any associate symptoms? Any dizziness, pleuritic chest pain, coughing, any sputum -Look at vital signs. Oxygenation problems might show low O2, increased heart rate, increased respiratory rate, increased temperature -Arterial blood gases are gold standard to tell about gas exchange... we only measure it if they are chronically ill (don't want to stick everyone's arteries) -Person could be pale, especially if anemia. Lips could turn blue/cyanotic. -Level of consciousness... will tell you if there's oxygen coming to the brain. If oxygenation is getting worse, they might be lethargic, confused, or agitated. -Respiratory assessment: auscultation, look at how person is breathing, are they using accessory muscles, any asymmetry in chest excursion, do they look distressed, listen and compare side to side, listen in enough places (5 lobes in the lung) , listen for adventitious sounds, listen for if the breath sounds are equal or diminished in certain areas, percuss -Cardiac assessment: heart and lungs are closely related, cap refill, listen to heart, taking pulse -Looking at periphery, are they edeamous? Fluid overload? -Think about what you're looking for
Pneumothorax: clinical manifestations
-Sudden onset of ipsilateral chest pain and dyspnea -Tachypnea -Unequal lung expansion -Diminished or absent breath sounds -Hyperresonance on percussion -Pretty abrupt; sudden onset of chest pain and SOB -Ipsilateral: same side as the problem -Tachypnea: rapid breathing -Unequal lung expansion if severe, you can observe by looking at them -Absent breath sounds -Hyperresoance: excess air
Lung cancer: medical treatment
-Surgery:Best chance of cure if tumor is resectable -Chemotherapy -Radiation -Targeted Therapies -Surgery best option for cure if tumor is accessible -Some tumors cannot be completely resected because of if they grow around major vessels, etc. -Chemo and radiation can play a role -New targeted therapies that stimulate the immune system to attack the tumor cells in terms of extending their lives
Pleural effusion: treatment
-Treat underlying cause -Thoracentesis -Pleurodesis -Treatment depends on why the fluid occurred in the first place -Resolve pulmonary infection or correct heart problems -Pleurodesis: inject something that irritates pleura and causes scar tissue to form and seals it off and stops effusions
Management of ARDS
-Treatment of Underlying Cause -Mechanical Ventilation with supplemental oxygen -Frequent Re-positioning -Hemodynamic Monitoring -Maintenance of Adequate CO -Maintenance of Fluid Balance -Maintenance of Nutrition -If septic, treat infection -High levels of oxygen -Frequent repositioning, rolling them over helps a lot to expand their lungs!! -Hemodynamic: perfusion and cardiac output -Maintain cardiac output -If dehydrated, perfusion worsens... but don't want too much fluid -Probably tube fed while on a ventilator
Hypercapnic
-Ventilatory failure -inability to eliminate CO2 -PaCO2 > 45 mm Hg and ph < 7.35 -Hypercapnic involves acid-base balance... CO2 is one of the ways body eliminates acid... if you cant get rid if CO2, you can't get rid of the acid -(Normal Co2 levels: 35-45) -Anything less than 7.35 is acidic
Cystic fibrosis
-Viscous Mucous -Recurrent Pulmonary Infections *Pseudomonas -Bronchiectasis -Pancreatic Insufficiency -Diagnosis: *Sweat Chloride Test *Genetic Testing -Median Survival Age 35 -Treatment *Chest Physiotherapy and Postural Drainage *Oxygen, antibiotics *Lung Transplant -Main problem: thick, sticky mucous... gets plugged up in lungs and starts to grow bacteria. Individual will get recurrent pulmonary infections. -Pseudomonas: results in nasty green pus -These infections start to damage the architecture of their bronchioles: bronchiectasis (damaged fibrous airways) -Measured chloride level of sweat (if higher than normal, its positive) -Now they just do genetic testing. -Used to be exclusively a pediatric problem because they didn't live to adulthood... now they do live. Median age is 35. -Management: control their pulmonary function... chest physiotherapy: a therapist will try to get the mucous to drain -Antibiotics for infection -Lung transplant can expand their life... their new lung will eventually develop the same problems
Asthama: clinical manifestations
-Wheezing -Cough -Dyspnea -Prolonged Expiration -Decreased Breath Sounds -Chest Tightness -Exercise-Induced -Wheezing: squeaky -Cough because bronchial spasm is irritating -SOB/dyspnea: airways narrow and tighten, harder to get air to come out during expiration phase; takes a long time to empty lungs -Diminished breath sounds due to tightening of airways -Feels chest tightness bc hard to get air in and out
IVC Filter
-inferior vena cava filter -Radiology suite. Make puncture in groin, thread up, deploy filter
Acute respiratory failure
-reoccuring PEs -minutes to hours
Chronic respiratory failure
-severe COPD where they can no longer oxygenate -several days or longer
Lung Volumes
-tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume -Breathe in and out, measuring -Tidal volume: amount of air that moves in and out during normal, relaxed breathing -Biggest, deepest breath to fill lungs = inspiratory reserve volume -Tidal volume + inspiratory reserve volume = inspiratory capacity (total volume of air you can pull into your lungs) -Expiratory reserve volume: blow out as much air as you can FVC: -Total lung capacity: total amount of air that can have inside Forced vital capacity: interested in if COPD or asthma
A nurse is teaching about examples of chronic obstructive pulmonary disease (COPD). Which diseases should the nurse include? Select all that apply.
Emphysema and Chronic Bronchitis Together, emphysema and chronic bronchitis are referred to as COPD because they often occur together. Asthma, pneumonia, and pulmonary fibrosis are not referred to as part of COPD.
Which person is most at risk for developing a pulmonary embolism?
A 67-year-old man with a deep vein thrombosis in the femoral vein The presence of deep vein thrombosis in the lower limbs is the most important risk factor for pulmonary embolism. Asthma is not a specific risk factor for pulmonary embolism. Although bone fracture and limb immobilization are risk factors for pulmonary embolism, most pulmonary emboli originate from the veins in the lower limbs. The risk of developing blood clots and pulmonary emboli after being immobilized for 1 week is not as high a risk factor as a deep vein thrombosis in the leg.
The amount of air inspired and expired during quiet breathing (about 500 ml) is called which of the following terms? A. Tidal volume B. Residual volume C. Vital Capacity D. Total Lung Capacity
A. Tidal Volume
The nurse teaches the patient about their asthma medications. Which statement by the patient indicates that they understand the teaching? A. I will rinse my mouth before I use the steroid inhaler B. I will use the Albuterol inhaler if I have acute symptoms C. I will use the steroid inhaler for quick relief D. If my symptoms worsen I will increase the dose of my steroid inhaler
B. I will use the Albuterol inhaler if I have acute symptoms Beta 2 agonist... opens up the lungs; rescuing inhaler Rinse mouth AFTER using steroid inhaler bc of residual of the steroid (can cause yeast) Never use maintenance inhaler for rescule Don't change dose without talking to provider
Lung cancer: metastasis
Brain, bone, liver *may have neurological issues if spread to brain
A patient is admitted with a large pulmonary embolism. The nurse recognizes that the patient is at risk for which of the following? A. Hypoxemic Respiratory Failure due to impaired diffusion B. Hypercapnic Respiratory Failure due to Alveolar hypoventilation C. Hypoxemic Respiratory Failure due to V/Q mismatch and intrapulmonary shunt D. Hypercapnic Respiratory Failure due to airway resistance
C. Hypoxemic Respiratory Failure due to V/Q mismatch and intrapulmonary shunt Large PE: severe VQ mismatch -> shunt
The nurse is caring for a patient with severe chronic COPD. There is an order to increase supplemental O2 from 1-4 liters. The first pulse ox is 89%. The nurse applies O2 at 4L NC. One hour later the patient is lethargic, his RR is 8 and the pulse ox is 79%. Which of the following actions should be done first? A. Increase the O2 flow rare B. Auscultate the lungs C. Stop the O2 D. Administer a bronchodilator
C. Stop the O2 CO2 retainer breaths off of their oxygen level If we give them too much oxygen, they can get worse because their brain thinks they have enough oxygen
What is the most common cause of a chronic cough in a client who smokes a pack of cigarettes a day?
Chronic bronchitis In persons who smoke, chronic bronchitis is the most common cause of chronic cough, although lung cancer must always be considered. Pulmonary embolus causes an acute cough, not a chronic cough. Asthma and postnasal drainage syndrome produce chronic coughs in individuals who do not smoke.
The client's previous medical records document a history of a reflex that helps clear the airways by an explosive expiration. What term should the nurse use to identify this respiratory behavior?
Cough Cough is a protective reflex that helps clear the airways by an explosive expiration. Paroxysmal nocturnal dyspnea is characterized by awaking at night gasping for air. Orthopnea is dyspnea that occurs when an individual lies flat; it is common in individuals with heart failure. Hypocapnia is defined as a Paco2 less than 36 mm Hg that can lead to respiratory alkalosis.
A patient has a large pleural effusion. Which physical exam finding would be expected? A. An expiratory wheeze B. Hyperresonance on percussion C. Course crackles D. Diminished breath sounds
D. Diminished breath sounds Fluid accumulating in pleural space... won't hear breath sounds in this area Wheezing - asthma and COPD Hyperresonance - too much air; pneumothorax or COPD Crackles - fluid inside the alveoli, not pleural space
A client presents to the primary care clinic complaining of breathlessness. The nurse also notes that the client is expending a great deal of effort to breathe. How should the nurse chart this finding?
Dyspnea present Dyspnea is often described as breathlessness, air hunger, shortness of breath, labored breathing, and preoccupation with breathing. Apnea is the absence of breathing. Tachypnea is a rapid ventilatory rate. Strenuous exercise or metabolic acidosis induces Kussmaul respiration (hyperpnea), which is characterized by a slightly increased ventilatory rate, very large tidal volumes, and no expiratory pause.
The nurse teaches a student nurse about the pathogenesis of bronchitis. Which information by the student indicates teaching was successful?
It is characterized by airway inflammation Bronchitis is characterized by airway inflammation as a result of inspired irritants. Hypersecretion of mucous along with a productive cough are seen for at least 3 months of the year for two consecutive years. There is a hyperresponsiveness to stimuli, not decreased.
Which client condition most commonly results in pulmonary edema?
Left-sided heart disease The most common cause of pulmonary edema is left-sided heart disease. When the left ventricle fails, filling pressures on the left side of the heart increase. Emphysema is abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis. Adequate surfactant would help prevent pulmonary edema. Dehydration would lead to a lack of fluids, not an excess.
A client lies flat and experiences dyspnea. Which term should the nurse use when charting?
Orthopnea Orthopnea is dyspnea that occurs when an individual lies flat and is common in individuals with heart failure. Cough is a protective reflex that helps clear the airways by an explosive expiration. Strenuous exercise or metabolic acidosis induces Kussmaul respiration (hyperpnea), which is characterized by a slightly increased ventilatory rate, very large tidal volumes, and no expiratory pause. Cyanosis is a bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin (which is bluish) in the blood.
A client reports awakening at night gasping for air and having to sit up to relieve difficult breathing. Which term should the nurse use to describe this finding?
Paroxysmal nocturnal dyspnea Some individuals with pulmonary or cardiac disease awaken at night gasping for air and have to sit up or stand to relieve the dyspnea (paroxysmal nocturnal dyspnea). Strenuous exercise or metabolic acidosis induces Kussmaul respiration (hyperpnea), which is characterized by a slightly increased ventilatory rate, very large tidal volumes, and no expiratory pause. Often the first dyspneic episode occurs with exercise and is called dyspnea on exertion. Hemoptysis is the expectoration of blood or bloody secretions.
What term should the nurse use to best describe accumulation of fluid in the client's pleural space?
Pleural effusion Pleural effusion is accumulation of fluid in the pleural space. Pleurisy is inflammation of the pleura that often manifests with pain on inspiration. A lung abscess is a circumscribed area of suppuration and lung tissue destruction. Flail chest is the chest movement during ventilation that results from the fracture of several consecutive ribs.
Which term should the nurse use to describe a client condition of excess water in the lung?
Pulmonary edema Pulmonary edema is excess water in the lung. Pneumonia is an infection in the lower lobes of the lung. Pneumoconiosis represents any change in the lung caused by inhalation of inorganic dust particles, usually in the workplace. Infection is not the term for excess water in the lung.
Differentiate rescue and maintenance inhaler
Rescue: Short-acting (Albuterol) Maintenance: Long-acting (Salmeterol)
When the nurse takes a health history, which finding will place the client at greatest risk for lung cancer?
Smoking Tobacco smoke contains more than 30 carcinogens and is responsible for causing 80% to 90% of lung cancers. Drinking, drug use, and sedentary lifestyle do not place the client at greater risk than smoking.
Which finding will cause the nurse to notify the primary healthcare provider for a client with asthma?
Status asthmaticus Status asthmaticus can be life-threatening if not reversed. The late phase response is part of the pathophysiology of asthma and is not always life-threatening. Mast cell degranulation is part of the pathophysiology of asthma and in itself is not life-threatening. Exercise-induced asthma is a form of asthma, rather than a complication of it.
A nurse is teaching a health and wellness class on reducing the risk for lung cancer. Which technique will the nurse suggest?
Stopping smoking The only proven way of reducing the risk for lung cancer is the cessation of smoking. Washing hands can prevent infection but not cancer. Cooking food thoroughly can prevent food poisoning but not lung cancer. Using safe sex practices can prevent sexually transmitted infections, but it does not reduce the risk for lung cancer.
When a nurse is caring for a client with Mycobacterium tuberculosis. Which principle of transmission should the nurse use to guide nursing care?
Transmitted by contact with infected airborne droplets Tuberculosis is spread by airborne droplets that are inhaled. The acid-fast bacillus is not transmitted via infected blood, sputum, or gastric secretions.
ARDS CXR
White-out x-ray Lungs full of fluid due to damage